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Pathology II > Dermatopathology (Part 2) > Flashcards

Dermatopathology (Part 2) Flashcards

1
Q

Inflammatory blistering disorders

A
  • Pemphigus
  • Bullous Pemphigoid
  • Dermatitis Herpetiformis
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2
Q

Noninflammatory blistering disorders

A
  • Epidermolysis Bullosa

- Porphyria

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3
Q

Subcorneal blisters

A
  • Stratum corneum forms the roof of the bulla (as in pemphigus foliaceus)
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4
Q

Suprabasilar blister

A
  • Portion of the epidermis, including the stratum corneum, forms the roof (as in pemphigus vulgaris)
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5
Q

Subepidermal blister

A
  • The entire epidermis separates from the dermis (as in bullous pemphigoid)
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6
Q

Pemphigus

A
  • Etiological factor = autoantibodies

- Result in the dissolution of intercellular attachments (epidermis, mucosal epithelium)

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7
Q

Pemphigus in adults

A
  • Fourth to 6th decades of life

- Men and women are affected equally

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8
Q

Multiple variants of pemphigus

A
  • Pemphigus vulgaris
  • Pemphigus vegetans
  • Pemphigus foliaceus
  • Pemphigus erythematosus
  • Paraneoplastic pemphigus
  • Disorders are benign
  • Extreme cases can be fatal without treatment
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9
Q

Pemphigus vulgaris

A
  • Most common type (80% of cases worldwide)
  • Mucosa
  • Skin
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10
Q

Pemphigus vulgaris affects the skin

A
  • Scalp
  • Face
  • Axilla
  • Groin
  • Trunk
  • Points of pressure
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11
Q

Pemphigus vulgaris as oral ulcers

A
  • Persist for months before skin involvement appears
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12
Q

Pemphigus vulgaris primary lesions

A
  • Superficial vesicles and bullae that rupture easily

- Shallow erosions covered with dried serum and crust

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13
Q

Pemphigus foliaceus

A
  • Benign form (endemic in Brazil; fogo selvagem)
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14
Q

Pemphigus foliaceus sites of predilection

A
  • Scalp
  • Face
  • Chest
  • Back
  • Mucous membranes (rarely affected)
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15
Q

Pemphigus folaceus bullae

A
  • Blisters found in the superficial epidermis at the level of the stratum granulosum
  • Present as areas of erythema and crusting
  • Erosions of previous blister rupture
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16
Q

Common histologic feature of all forms of Pemphigus

A
  • Acantholysis
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17
Q

Acantholysis in pemphigus

A
  • Dissolution or lysis of the intercellular bridges
  • Pemphigus vulgaris and Pemphigus vegetans
  • Acantholysis selectively involves the cells immediately above the basal cell layer
  • Suprabasal acantholytic blister
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18
Q

Pemphigus pathogenesis (autoimmune)

A
  • IgG autoantibodies against desmogleins
  • Disruption of intercellular adhesions
  • Result – Blisters formation
  • Direct immunofluorescence
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19
Q

Direct immunofluorescence in pemphigus

A
  • Net-like pattern of intercellular IgG deposits
  • Pemphigus vulgaris = IgG is usually seen at all levels of the epithelium in
  • Pemphigus foliaceus = IgG distribution is superficial
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20
Q

Pemphigus vulgaris depositis

A
  • Deposition of Ab along the plasma membranes of keratinocytes in a reticular pattern
  • Accompanied by suprabasalar loss of cell-to-cell adhesion (acantholysis)
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21
Q

Pemphigus foliaceus deposits

A
  • Ab deposits and acantholysis are more superficial
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22
Q

Bullous pemphigoid

A
  • Affects the elderly

- Orla lesions

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23
Q

Bullous pemphigoid sites of involvement

A
  • Inner aspects of the thighs
  • Flexor surfaces of the forearms
  • Axillae
  • Groin
  • Lower abdomen
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24
Q

Bullous pemphigoid oral lesions

A
  • Present in 10% to 15% of affected individuals
  • Appear after the cutaneous lesions
  • Patients may present with urticarial plaques and severe pruritus
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25
Q

Bullous pemphigoid pathogenesis

A
  • Autoantibodies binding to hemidesmosome proteins
  • Linear deposition pattern at dermoepidermal junction
  • Antibodies against BPAG2 cause blistering
  • Autoantibodies activate complement
  • Recruitment
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26
Q

Bullous pemphigoid antigens (BPAGs)

A
  • Components of hemidesmosomes
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27
Q

Bullous pemphigoid recruits

A
  • Neutrophils

- Eosinophils (inflammation and disruption of epidermal attachments)

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28
Q

Bullous pemphigoig morpology (1)

A
  • Tense bullae filled with clear fluid
  • Bullae are usually less than 2 cm in diameter (can reach 4 to 8 cm)
  • Bullae do not rupture easily
  • Heal without scarring
  • Distinguishing Characteristic
  • Subepidermal, nonacantholytic blisters
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29
Q

Bullous pemphigoig morphology (2)

A
  • Deep perivascular infiltrate (lymphocytes, eosinophils, neutrophils)
  • Superficial dermal edema
  • Basal cell layer vacuolization
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30
Q

Dermatitis herpetiformis characteristics

A
  • Rare
  • Urticaria
  • Vesicles (pruritic)
  • Affects predominantly males
  • Third and fourth decades of life
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31
Q

Dermatitis herpetiformis asociations

A
  • Intestinal celiac disease
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32
Q

Dermatitis herpetiformis pathogenesis

A
  • Genetic predisposition
  • Individuals develop lgA Abs to dietary gluten
  • Abs cross-react with reticulin
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33
Q

Abs cross-react with reticulin (dermatitis herpetiformis)

A
  • Component of the anchoring fibrils

- Resultant subepidermal blister develops

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34
Q

Dermatitis herpetiformis lesions

A
  • Bilateral
  • Symmetric
  • Grouped
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35
Q

Dermatitis herpetiformis areas involved

A
  • Extensor surfaces
  • Elbows
  • Knees
  • Upper back
  • Buttocks
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36
Q

Dermatitis herpetiformis morphology

A
  • Fibrin and neutrophils accumulate at tips of dermal papillae
  • Small microabscesses
  • Direct Immunofluorescence (discontinuous, granular deposits of lgA at tips of dermal papillae)
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37
Q

Epidermolysis bullosa

A
  • Inherited defects in structural proteins
  • Formation of Blisters
  • Sites of pressure
  • Friction
  • Trauma
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38
Q

Epidermolysis bullosa simplex type

A
  • Autosomal dominant mode of inheritance
  • Mutations in genes encoding keratin 14 or 5
  • Pair with one another to make a functional keratin fiber
  • Basal cell layer defect
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39
Q

Epidermolysis bullosa simplex

Weber-Cockayne subtype

A
  • Mild bullous disease

- Characterized by localized blistering at sites of trauma such as the feet

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40
Q

Dermatitis herpetiformis

blisters are associated with

A
  • Accumulation of neutrophils (microabscesses) at the tips of dermal papillae
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41
Q

Epidermolysis bullosa simplex

Koebner subtype

A
  • Palmoplantar blistering and hyperkeratosis are noted

- Hyperkeratotic papules and plaques on the palm

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42
Q

Epidermolysis bullosa junctional type

A
  • Blisters of normal skin at the lamina lucida
  • Autosomal recessive defect
  • Subunits of laminin
  • Binds to hemidesmosomes and anchoring filaments
  • Typical erosions in flexural creases
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43
Q

Junctional epidermolysis bullosa (Herlitz subtype)

A
  • Severe disease characterized by generalized intralamina lucida blistering at birth
  • Significant internal involvement
  • Poor prognosis
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44
Q

Dystrophic Epidermolysis Bullosa

A
  • Sublamina densa BMZ separation
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45
Q

Hemidesmosomal Epidermolysis Bullosa

New category

A
  • Produces blistering at the hemidesmosomal level
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46
Q

Dominantly inherited dystrophic epidermolysis bullosa

A
  • Blistering often is localized and is characterized by scarring and milia in healed blister sites
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47
Q

Dominantly inherited dystrophic epidermolysis bullosa can result in

A
  • Nail dystrophy and loss

oral cavity blistering and scarring

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48
Q

Epidermolysis bullosa types

A
  • Epidermolysis bullosa simplex (intraepidermal skin separation)
  • Junctional epidermolysis bullosa (skin separation in lamina lucida or central BMZ)
  • Dystrophic epidermolysis bullosa (sublamina densa BMZ separation)
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49
Q

Junctional Epidermolysis Bullosa histology

A
  • Subepidermal blister at the level of the lamina lucida

- No associated inflammation

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50
Q

Acne vulgaris

A
  • Teenagers
  • Affects both males and females
  • Males tend to have more severe disease
  • Induced or exacerbated by drugs
  • Noninflammatory/inflammatory
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51
Q

Drugs that exacerbate or induce acne

A
  • Corticosteroids
  • Adre­nocorticotropic hormone
  • Testosterone
  • Gonadotropins
  • Contraceptives
  • Trimethadione
  • Iodides
  • Bromides
52
Q

Acne vulgaris occupational exposures/conditions favoring sebaceous gland occlusion

A
  • Heavy clothing
  • Cosmetics
  • Tropical climates
  • Familial
53
Q

Acne vulgaris open comedones

A
  • Small follicular papules
  • Contain a central black keratin plug
  • Color is the result of melanin pigment oxidation
54
Q

Acne vulgaris closed comedones

A
  • Follicular papules without a visible central plug
  • Keratin plug trapped beneath the epidermal surface
  • Potential sources of follicular rupture and inflammation
55
Q

Acne vulgaris grade I

A
  • Multiple open comedones
56
Q

Acne vulgaris grade II

A
  • Closed comedones
57
Q

Acne vulgaris pathogenesis (incompletely understood/multifactorial) contributing factors

A
  • Development of a keratin plug that blocks outflow of sebum
  • Hypertrophy of sebaceous glands during puberty
  • Lipids converted to proinflammatory fatty acids (probionibacterium acnes)
58
Q

Inflammatory acne vulgaris

A
  • Erythematous papules, nodules, and pustules
  • Severe Variants
  • Acne conglobata
  • Result in sinus tract formation and dermal scarring
  • Deep inflammatory nodules may develop
59
Q

Inflammatory acne characteristics

A
  • Open Comedones (large, patulous orifices)
  • Closed comedones (microscopic identification only)
  • Variable infiltrates of lymphocytes and macrophages around affected follicles
  • Extensive acute inflammation (occurs with follicular rupture)
  • Dermal abscesses may form in association with rupture
60
Q

Acne vulgaris grade III

A
  • Papulopustules
61
Q

Acne vulgaris grade IV

A
  • Multiple open comedones, closed comedones, and papulopustules
  • Plus cysts
62
Q

Rosacea

A
  • Common disease of middle age and beyond
  • Affects up to 3% of the US population
  • Pre­dilection for females
63
Q

Rosacea four stages

A
  • Flushing episodes (pre-rosacea)
  • Persistent erythema and telangiectasia
  • Pustules and papules
  • Rhinophyma
64
Q

Rhinophyma

A
  • Permanent thickening of the nasal skin
  • Confluent erythematous papules
  • Prominent follicles
65
Q

Rosacea pathogenesis

A
  • High cutaneous levels of cathelicidin (AMP)

- Cathelicidin peptides distinct from individuals without rosace

66
Q

Cathelicidin peptides in rosacea

A
  • Expressed by PMNs and lymphocytes
  • Stimulates angiogenesis
  • Induces inflammation
  • Telangiectasia formation
67
Q

Rosacea morphology

A
  • Nonspecific perifollicular lymphocytic infiltrate
  • Lymphocytes surrounded by dermal edema and telangiectasia
  • Pustular Phase
68
Q

Pustular phase of rosacea morphology

A
  • Neutrophils may colonize the follicles
  • Follicular rupture may cause a granulomatous dermal response
  • Development of Rhinophyma
69
Q

Rhinophyma (rosacea pustular phase)

A
  • Hypertrophy of sebaceous glands

- Follicular plugging by keratotic debris

70
Q

Panniculitis

A
  • Inflammatory reaction in the subcutaneous adipose tissue
  • Preferentially affect
  • Lobules of fat
  • Connective tissue that separates fat into lobules
  • Involves the lower legs
71
Q

Panniculitis forms

A
  • Erythema nodosum (most common)

- Erythema induratum (uncommon)

72
Q

Erythema induratum (uncommon)

A
  • Affects adolescents and menopausal women
  • Cause is not known
  • Vasculitis of deep vessels supplying the fat lobules of the subQ
  • Vascular compromise leads to fat necrosis and inflammation
  • Presents as an erythe­matous, slightly tender nodule that usually ulcerates
73
Q

Erythema nodosum

A
  • Poorly defined, tender, erythematous plaques and nodules

- Associated Infections

74
Q

Associated infections with erythema nodosum

A
  • β-hemolytic streptococcal infection

- Tuberculosis

75
Q

Erythema nodosum (panniculitis) drug administration

A
  • Sulfonamides

- Oral contraceptives

76
Q

Erythema nodosum (panniculitis) conditions

A
  • Sarcoidosis
  • Inflammatory bowel disease
  • Malignant neoplasms
77
Q

Erythema nodosum pathogenesis

A
  • Remains mysterious
  • DTH reaction to microbial or drug related antigens
    Immune complexes have been implicated
78
Q

Erythema nodosum clinical presentation

A
  • Fever and malaise may accompany the cutaneous signs
79
Q

Panniculitis early lesions morphology

A
  • Connective tissue septae are widened by edema, fibrin exudation, and neutrophilic infiltration
80
Q

Panniculitis later lesions morphology

A
  • Septal fibrosis

- Infiltration (lymphocytes, histiocytes, multinucleated giant cells, eosinophils)

81
Q

Classic presentation of erythema nodosum

A
  • Nodular red swellings over the shins
82
Q

Erythema induratum

A
  • Tender, erythematous nodules confined to the lower third of the legs
  • Panniculitis exhibiting lobular, granulomatous, and lymphohistiocytic inflammation
83
Q

Positive Mantoux test

A
  • Reaction in a patient with erythema induratum
84
Q

Verrucae (warts)

A
  • Squamoproliferative disorders caused by HPV

- Common lesions of children and adolescents

85
Q

Verrucae (warts) transmission

A
  • Direct contact between individuals or autoinoculation
  • Self-limited
  • Regress spontaneously / 6 months to 2 years
86
Q

Verrucae (warts) clinical variants (associated with distinct HPV subtypes)

A
  • HPV types 1-4
  • HPV types 6 and 11
  • HPV type 16
87
Q

Verrucae associated with HPV types 1 – 4

A
  • Common warts on hands and feet
88
Q

Verrucae associated with HPV types 6 and 11

A
  • Anogenital warts (Condyloma accuminatum)
89
Q

Verrucae associated with HPV type 16

A
  • In situ squamous cell carcinoma of the genitalia

- Bowenoid papulosis

90
Q

Verruca vulgaris

A
  • Most common
  • Occur frequently on hands (dorsal surfaces, periungual areas)
  • Appear as gray-white to tan
    Flat to convex (0.1- to 1-cm papules with a rough, pebble-like surface)
91
Q

Verruca plana

A
  • Flat wart
  • Common on face
  • Dorsal surfaces of the hands
  • Slightly elevated
  • Flat, smooth, tan papules
  • Smaller than verruca vulgaris
92
Q

Verruca Plantaris and Verruca Palmaris

A
  • Occur on the soles and palms
  • Rough, scaly lesions
  • 1 to 2 cm
  • Coalesce
  • Confused with calluses
93
Q

Condyloma Acuminatum (Venereal wart)

A
  • Penis
  • Female genitalia
  • Urethra
  • Perianal areas
  • Rectum
  • Soft, tan, cauliflower-like masses
  • Can reach many centimeters in diameter
94
Q

Common histological features of verrucae

A
  • Epidermal hyperplasia
  • Undulant in character, termed verrucous or papillomatous epidermal hyperplasia
  • Cytoplasmic vacuolization (Koilocytosis)
95
Q

Cytoplasmic vacuolization (Koilocytosis)

A
  • Involving the more superficial epidermal layers

- Haloes of pallor surrounding infected nuclei

96
Q

Molluscum contagiosum

A
  • Common
  • Self-limited viral disease
  • Cause / poxvirus
  • Infection is usually spread by direct contact
97
Q

Molluscum contagiosum multiple lesions

A
  • Skin and mucous membranes

- Predilection for the trunk and anogenital areas

98
Q

Molluscum contagiosum lesion characteristics

A
  • Firm, pruritic
  • Pink to skin-colored
  • Umbilicated papules
  • Range from 0.2 cm to 0.4 cm
  • Curd-like material expressed from central umbilication
  • Material contains diagnostic molluscum bodies
99
Q

Molluscum contagiosum microscopic examination

A
  • Cuplike verrucous epidermal hyperplasia
  • Diagnostic structure is the molluscum body
  • H&E Stains
100
Q

Diagnostic structure is the molluscum body

A
  • Large (up to 35 µm), ellipsoid, homogeneous, cytoplasmic inclusion
  • Cells of the stratum granulosum and the stratum corneum
101
Q

H&E stains

A
  • Eosinophilic in the blue-purple stratum granulosum
  • Acquire a pale blue hue in the red stratum corneum
  • Numerous virions are present within molluscum bodies
102
Q

Impetigo

A
  • Superficial bacterial infection of skin
  • Highly contagious
  • Causative agent – S. aureus
103
Q

Impetigo two forms

A
  • Impetigo contagiosa
  • Impetigo bullosa
  • Differ by the size of the pustules
104
Q

Impetigo pathogenesis

A
  • Innate immune response
  • Responsible for epidermal injury
  • Serous exudate and formation of a scale crust (scab)
  • Bacterial toxin that cleaves desmoglein 1
105
Q

Impetigo presentation

A
  • Erythematous macule
  • Multiple small pustules
  • Shallow erosions
  • Covered with dry serum
106
Q

Impetigo characteristic appearance

A
  • Honey-colored crust

- Bullous forms occur in children

107
Q

Impetigo microscopic featur

A
  • Accumulation of neutrophils beneath the stratum corneum
  • Often producing a subcorneal pustule (containing serum protein, inflammatory cells)
  • Special stains reveal the presence of bacteria in these foci
108
Q

Superficial fungal infections basic characteristics

A
  • Confined to the stratum corneum

- Caused by dermatophytes

109
Q

Tinea capitis (superficial fungal infection)

A
  • Commonly seen in children
  • Rarely in infants and adults
  • Dermatophytosis of the scalp
  • Asymptomatic
  • Presents as hairless patches of skin
110
Q

Tinea capitis associated with

A
  • Mild erythema
  • Crust formation
  • Scaling
111
Q

Tinea barbae

A
  • Dermatophyte infection of the beard area
  • Affects adult men
  • Uncommon disorder
112
Q

Tinea corporis

A
  • Superficial fungal infection of the body surface
  • Affects persons of all ages
  • Particularly children
113
Q

Tinea corporis predisposing factors

A
  • Excessive heat
  • High humidity
  • Exposure to infected animals
  • Chronic dermatophytosis of the feet or nails
114
Q

Tinea corporis (Ringworm)

A
  • Expanding, round, slightly erythematous plaque

- Elevated scaling border

115
Q

Tinea cruris (Jock Itch)

A
  • Inguinal areas
  • Obese men
  • Athletes
116
Q

Tinea cruris (jock itch) predisposing factors

A
  • Heat
  • Friction
  • Maceration
117
Q

Tinea cruris (jock itch) appearance

A
  • Appears on the upper inner thighs

- Moist, red patches with raised scaly borders

118
Q

Tinea pedis (Athlete’s foot)

A
  • Affects 30% to 40% of the population
  • Diffuse erythema and scaling
  • Initially localized to the web spaces
  • Inflammatory reaction (result of bacterial superinfection)
119
Q

Tinea pedis (Athlete’s foot) may involve finger and toenails

A
  • Onchomycosis
  • Discoloration
  • Thickening
  • Deformed nail plate
120
Q

Tinea pedis (athlete’s foot) appearance

A
  • Diffuse erythema and scaling
  • Initially localized to the web spaces
  • Inflammatory reaction
121
Q

Tinea versicolor

A
  • Occurs on the upper trunk
  • Causative agent = Malassezia furfur (a yeast, not a dermatophyte)
  • Lesions = groups of macules of varied size and color
  • Fine peripheral scaling
122
Q

Tinea versicolor morpholoy

A
  • Mild eczematous dermatitis
    Intraepidermal neutrophils
  • Periodic acid–Schiff stain (bright pink to red)
  • Found in the anucleate cornified layer
  • Scrapes use to identify offending species
123
Q

Lichen planus cutaneous lesions morphology

A
  • Darkly pigmented individuals (melanin release into the dermis, basal cell layer destruction)
  • Lesions / multiple and symmetrically distributed
  • Extremities, wrists, elbows
  • Oral lesions (white, reticulated, or netlike)
124
Q

Porphyria

A
  • Disturbances of porphyrin metabolism

- Porphyrins (Pigments): hemoglobin, myoglobin, cytochromes

125
Q

Classification of porphyrias (based on both clinical and biochemical features)

A
  • Congenital erythropoietic porphyria
  • Erythrohepatic protoporphyria
  • Acute intermittent porphyria
  • Porphyria cutanea tarda
  • Mixed porphyria
126
Q

Cutaneous manifestations of porphyria

A
  • Urticaria and vesicles
  • Associated scarring
  • Condition exacerbated by sunlight exposure
  • Vesicles have subepidermal location
  • Pathogenesis not understood

Pathology II (7 decks)

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