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GBA Pathology > PATHOMA19 - Skin Pathology > Flashcards

PATHOMA19 - Skin Pathology Flashcards

1
Q

What is the function of skin?

A

It is a barrier against environmental insults and fluid loss

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2
Q

What is skin composed of?

A

an epidermis and dermis

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3
Q

What is the epidermis comprised of?

A

keratinocytes and has four layers

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4
Q

What are the layers of the epidermis?

A

1) Stratum basalis 2) Stratum spinosum 3) Stratum granulosum 4) Stratum corneum

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5
Q

What is the stratum basalis?

A

regenerative (stem cell) layer

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6
Q

What is the stratum spinosum?

A

Its characterized by desmosomes between keratinocytes

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7
Q

What is the stratum granulosum?

A

It is characterized by granules in keratinocytes

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8
Q

What is the stratum corneum?

A

It is characterized by keratin in anucleate cells

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9
Q

What does the dermis consist of?

A

connective tissue, nerve endings, blood and lymphatic vessels, and adnexal structures (e.g., hair shafts, sweat glands, and sebaceous glands)

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10
Q

What are the inflammatory dermatoses?

A

1) atopic (eczematous) dermatitis 2) contact dermatitis 3) acne vulgaris 4) psoriasis 5) Lichen Planus

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11
Q

What is atopic (eczematous) dermatitis?

A

Pruritic, erythematous, oozing rash with vesicles and edema; often involves the face and flexor surfaces

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12
Q

What are flexor surfaces?

A

Elbow, wrists and knees

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13
Q

What is type 1 hypersensitivity reaction associated with?

A

asthma and allergic rhinitis

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14
Q

What is contact dermatitis?

A

Pruritic, erythematous, oozing rash with vesicles and edema

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15
Q

When does contact dermatitis arise?

A

upon exposure to allergens

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16
Q

What are the allergens for contact dermatitis?

A

1) Poison ivy and nickel jewelry (type IV hypersensitivity) 2) Irritant chemicals (e.g., detergents) 3) Drugs (e.g., penicillin)

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17
Q

What is the treatment for contact dermatitis?

A

It involves removal of the offending agent and topical glucocorticoids, if needed.

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18
Q

What is acne vulgaris?

A

Comedones (whiteheads and blackheads), pustules (pimples), and nodules; extremely common, especially in adolescents

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19
Q

What is acne vulgaris due to?

A

chronic inflammation of hair follicles and associated sebaceous glands

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20
Q

In acne vulgaris, how are comedones formed?

A

There is hormone-associated increase in sebum production (sebaceous glands have androgen receptors) and excess keratin production block follicles

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21
Q

What are propionibacterium acnes?

A

It is infection that produces lipases that break down sebum, releasing proinflammatory fatty acids; results in pustule or nodule formation

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22
Q

What is the treatment for acne vulgaris?

A

Treatment includes benzoyl peroxide (antimicrobial) and vitamin A derivatives (e.g., isotretinoin), which reduce keratin production.

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23
Q

What is psoriasis?

A

Well-circumscribed, salmon-colored plaques with silvery scale, usually on extensor surfaces and the scalp; pitting of nails may also be present.

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24
Q

What is psoriasis due to?

A

excessive keratinocyte proliferation

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25
Q

What is the etiology for psoriasis?

A

Possible autoimmune etiology

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26
Q

What is psoriasis associated with?

A

HLA-C

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27
Q

For psoriasis, what happens if there is an environmental trigger?

A

lesions often arise in areas of trauma (environmental trigger)

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28
Q

What does the histology for psoriasis show?

A

1) Acanthosis (epidermal hyperplasia) 2) Parakeratosis 3) Collections of neutrophils in the stratum corneum (Munro microabscesses) 4) Thinning of the epidermis above elongated dermal papillae; results in bleeding when scale is picked off (Auspitz sign)

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29
Q

What is parakeratosis?

A

hyperkeratosis with retention of keratinocyte nuclei in the stratum comeum

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30
Q

What is the treatment for psoriasis?

A

it involves corticosteroids, UV light with psoralen, or immune-modulating therapy.

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31
Q

What is lichen planus?

A

Pruritic, planar, polygonal, purple papules often with reticular white lines on their surface (Wickham striae); commonly involves wrists, elbows, and oral mucosa

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32
Q

What does lichen planus commonly involve?

A

Wrists, elbows and oral mucosa

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33
Q

What does oral involvement of lichen planus manifest as?

A

Wickham striae

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34
Q

What does histology for lichen planus show?

A

inflammation of the dermal-epidermal junction with a saw-tooth appearance

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35
Q

What is the etiology for lichen planus?

A

Etiology is unknown

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36
Q

What is lichen planus associated with?

A

chronic hepatitis C virus infection

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37
Q

What are the blistering dermatoses?

A

1) pemphigus vulgaris 2) bullous phemphigoid 3) dermatitis herpetiformois 4) erythema multiforme

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38
Q

What is pemphigus vulgaris?

A

Its autoimmune destruction of desmosomes between keratinocytes

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39
Q

What is pemphigus vulgaris due to?

A

IgG antibody against desmoglein (type II hypersensitivity)

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40
Q

What does pemphigus vulgaris present as?

A

skin and oral mucosa bullae

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41
Q

In pemphigus vulgaris, why is there suprabasal blisters?

A

Acantholysis (separation) of stratum spinosum keratinocytes (normally connected by desmosomes) results in suprabasal blisters.

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42
Q

In pemphigus vulgaris, why is there a tombstone appearance?

A

Basal layer cells remain attached to basement membrane via hemidesmosomes - tombstone appearance

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43
Q

In pemphigus vulgaris, why is there shallow erosions with dried crust?

A

Thin-walled bullae rupture easily (Nikolsky sign), leading to shallow erosions with dried crust.

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44
Q

In pemphigus vulgaris, why is there a fish net pattern?

A

Immunofluorescence highlights IgG surrounding keratinocytes in a fish net pattern.

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45
Q

What is bullous pemphigoid?

A

Autoimmune destruction of hemidesmosomes between basal cells and the underlying basement membrane

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46
Q

What is bullous pemphigoid due to?

A

Its due to IgG antibody against basement membrane collagen

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47
Q

What does bullous pemphigoid present as?

A

blisters of the skin, oral mucosa is spared 1) Basal cell layer is detached from the basement membrane 2) Tense bullae do not rupture easily; clinically milder than pemphigus vulgaris

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48
Q

In bullous pemphigoid, what does immunofluorescence show?

A

it highlights IgG along basement membrane (linear pattern)

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49
Q

What is dermatitis herpetiformis?

A

Autoimmune deposition of IgA at the tips of dermal papillae

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50
Q

What does dermatitis herpetiformis present?

A

as pruritic vesicles and bullae that are grouped (herpetiform)

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51
Q

Dermatitis herpetiformis has a strong association with what?

A

celiac disease; resolves with gluten-free diet

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52
Q

What is erythema multiforme?

A

Hypersensitivity reaction characterized by targetoid rash and bullae

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53
Q

What is the targetoid appearance due to?

A

central epidermal necrosis surrounded by erythema

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54
Q

Erythema multiforme is most commonly associated with what?

A

HSV infection

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55
Q

Aside form HSV infections, what do the other associations include?

A

Mycoplasma infection, drugs (penicillin and sulfonamides), autoimmune disease (eg SLE), and malignancy

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56
Q

What is Steven Johnsons syndrome?

A

EM with oral mucosa/lip involvement and fever is termed Stevens Johnson syndrome (SJS)

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57
Q

What is toxic epidermal necrolysis?

A

It is a severe form of SJS characterized by diffuse sloughing of skin, resembling a large bum; most often due to an adverse drug reaction

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58
Q

What are the epithelial tumors?

A

1) seborrheic keratosis 2) acanthosis nigracans 3) basal cell carcinoma 4) squamous cell carcinoma

59
Q

What is seborrheic keratosis?

A

Benign squamous proliferation; common tumor in the elderly

60
Q

What does seborrheic keratosis present as?

A

raised, discolored plaques on the extremities or face; often has a coinlike, waxy, stuck-on appearance

61
Q

What is seborrheic keratosis characterized by?

A

keratin pseudocysts on histology

62
Q

What is a sign involved with seborrheic keratosis?

A

Leser-Trelat sign is the sudden onset of multiple seborrheic keratoses and suggests underlying carcinoma of the GI tract

63
Q

What is acanthosis nigricans?

A

Epidermal hyperplasia with darkening of the skin, velvet-like skin; often involves the axilla or groin

64
Q

What is acanthosis nigricans associated with?

A

insulin resistance (e.g., non-insulin-dependent diabetes) or malignancy (especially gastric carcinoma)

65
Q

What is basal cell carcinoma?

A

Malignant proliferation of the basal cells of the epidermis

66
Q

What is the most common cutaneous malignancy?

A

Basal cell carcinoma

67
Q

What are the risk factors for basal cell carcinoma?

A

stem from UVB-induced DNA damage and include prolonged exposure to sunlight, albinism, and xeroderma pigmentosum

68
Q

What does basal cell carcinoma present as?

A

an elevated nodule with a central, ulcerated crater surrounded by dilated (telangiectatic) vessels, pink, pearl-like papule

69
Q

What is the classic location for basal cell carcinoma?

A

Classic location is the upper lip

70
Q

What does the histology for basal cell carcinoma show?

A

nodules of basal cells with peripheral palisading

71
Q

What is the treatment for basal cell carcinoma?

A

surgical excision; metastasis is rare.

72
Q

What is squamous cell carcinoma?

A

malignant proliferation of squamous cells

73
Q

What is squamous cell carcinoma characterized by?

A

formation of keratin pearls

74
Q

What are the risk factors for squamous cell carcinoma?

A

stem from UVB-induced DNA damage and include prolonged exposure to sunlight, albinism, and xeroderma pigmentosum.

75
Q

What are the additional risk factors for squamous cell carcinoma?

A

they include immunosuppressive therapy, arsenic exposure, and chronic inflammation (eg scar from burn or draining sinus tract)

76
Q

What does squamous cell carcinoma present as?

A

an ulcerated, nodular mass, usually on the face (classically involving the lower lip)

77
Q

What is the treatment for squamous cell carcinoma?

A

it is excision; metastasis is uncommon.

78
Q

What is a precursor lesion of squamous cell carcinoma and how does it present?

A

Actinic keratosis and presents as a hyperkeratotic, scaly plaque, often on the face, back, or neck.

79
Q

What is Keratoacanthoma?

A

it is well-differentiated squamous cell carcinoma that develops rapidly and regresses spontaneously

80
Q

How does keratoacanthoma present?

A

as a cup-shaped tumor filled with keratin debris

81
Q

What are the disorders of pigmentation and melanocytes?

A

1) vitiligo 2) albinism 3) Freckle (ephelis) 4) melasma 5) nevus (mole) 6) melanoma

82
Q

What are melanocytes responsible for?

A

skin pigmentation

83
Q

Where are melanocytes located?

A

They are present in the basal layer of the epidermis.

84
Q

What are melanocytes derived from?

A

the neural crest

85
Q

What do melanocytes do?

A

Synthesize melanin in melanosomes using tyrosine as a precursor molecule

86
Q

What do melanocytes do?

A

They pass melanosomes to keratinocytes

87
Q

What is vitiligo?

A

Localized loss of skin pigmentation

88
Q

What is vitiligo due to?

A

autoimmune destruction of melanocytes

89
Q

What happens in albinism?

A

It is a congenital lack of pigmentation

90
Q

What is albinism due to?

A

an enzyme defect (usually tyrosinase) that impairs melanin production

91
Q

What might albinism involve?

A

May involve the eyes (ocular form) or both the eyes and skin (oculocutaneous form)

92
Q

What is there an increased risk for in albinism and why?

A

Increased risk of squamous cell carcinoma, basal cell carcinoma, and melanoma due to reduced protection against UVB

93
Q

What is freckle?

A

(ephelis) small, tan to brown macule; darkens when exposed to sunlight

94
Q

What is freckle due to?

A

increased number of melanosomes (melanocytes are not increased)

95
Q

What is melasma?

A

mask-like hyperpigmentation of the cheeks

96
Q

What is melasma associated with?

A

pregnancy and oral contraceptives

97
Q

What is nevus?

A

(mole) benign neoplasm of melanocytes

98
Q

What is congenital nevus?

A

it is present at birth; often associated with hair

99
Q

When do you see acquired nevus?

A

it arises later in life.

100
Q

How does a nevus begin?

A

Begins as nests of melanocytes at the dermal-epidermal junction (junctional nevus);

101
Q

What is the most common mole in children?

A

nevus

102
Q

What is a compound nevus?

A

When the nevus grows by extension into the dermis

103
Q

What is an intradermal nevus?

A

The junctional component is eventually lost resulting in an intradermal nevus, which is the most common mole in adults.

104
Q

What is the most common mole in adults?

A

Intradermal nevus

105
Q

What is a nevus characterized by?

A

Characterized by a flat macule or raised papule with symmetry, sharp borders, evenly distributed color, and small diameter (< 6 mm)

106
Q

What might arise from a nevus?

A

Dysplasia may arise (dysplastic nevus), which is a precursor to melanoma

107
Q

What is melanoma?

A

Malignant neoplasm of melanocytes; most common cause of death from skin cancer

108
Q

What is the most common form of death from skin cancer?

A

Melanoma

109
Q

What are the risk factors for melanoma?

A

They are based on UVB-induced DNA damage and include prolonged exposure to sunlight, albinism, and xeroderma pigmentosum; an additional risk factor is dysplastic nevus syndrome,

110
Q

What is dysplastic nevus syndrome?

A

autosomal dominant disorder characterized by formation of dysplastic nevi that may progress to melanoma

111
Q

What does dysplastic nevus syndrome present as?

A

a mole-like growth with ABCD

112
Q

What is the ABCD for a mole like growth in dysplastic nevus syndrome?

A

1) Asymmetry 2) Borders are irregular. 3) Color is not uniform. 4) Diameter > 6 mm

113
Q

How is melanoma characterized?

A

by two growth phases

114
Q

What are the growth phases that characterize melanoma?

A

1) radial growth 2) vertical growth

115
Q

What is the radial growth in melanoma?

A

It grows horizontally along the epidermis and superficial dermis

116
Q

For radial growth, what is the risk for metastasis?

A

low risk of metastasis

117
Q

What is the vertical growth in melanoma?

A

It grows vertically into the deep dermis

118
Q

In vertical growth in melanoma what is the most important prognostic factor in predicting metastasis?

A

The depth of extension (Breslow thickness) is the most important prognostic factor in predicting metastasis.

119
Q

What are the variants for melanoma?

A

1) superficial spreading 2) lentigo maligna melanoma 3) nodular 4) acral lentiginous

120
Q

What is superficial spreading in melanoma?

A

most common subtype; dominant early radial growth results in good prognosis

121
Q

What is the prognosis for superficial spreading in melanoma?

A

Dominant early radial growth results in good prognosis

122
Q

What is lentigo maligna melanoma and what is the prognosis?

A

lentiginous proliferation (radial growth) good prognosis

123
Q

What is nodular regarding the variant of melanoma and what is the prognosis?

A

early vertical growth; poor prognosis

124
Q

What is involved in the Acral lentiginous variant of melanoma?

A

It arises on the palms or soles, often in dark-skinned individuals; not related to UV light exposure

125
Q

What is impetigo?

A

Superficial bacterial skin infection

126
Q

What is impetigo most often due to?

A

S. aureus or S. pyogenes

127
Q

Who does impetigo commonly affect?

A

children

128
Q

What does impetigo present as?

A

erythematous macules that progress to pustules, usually on the face; rupture of pustules results in erosions and dry, crusted, honey-colored serum.

129
Q

What is cellulitis?

A

It?s a deeper (dermal and subcutaneous) infection, usually due to S. aureus or S. pyogenes

130
Q

What does cellulitis present as?

A

a red, tender, swollen rash with fever

131
Q

What are the risk factors for cellulitis?

A

They include recent surgery, trauma, or insect bite.

132
Q

What can cellulitis progress to?

A

Can progress to necrotizing fasciitis with necrosis of subcutaneous tissues due to infection with anaerobic flesh-eating bacteria

133
Q

What happens when cellulitis progresses to necrotizing fasciitis?

A

1) Production of CO2 leads to crepitus. 2) Surgical emergency

134
Q

What is staphylococcal scaled skin syndrome?

A

Sloughing of skin with erythematous rash and fever; leads to significant skin loss

135
Q

What is staphylococcal scaled skin syndrome due to?

A

S. aureus infection; where there is exfoliative A and B toxins that result in epidermolysis of the stratum granulosum.

136
Q

How is staphylococcal scaled skin syndrome distinguished histologically from toxic epidermal necrolysis?

A

by level of skin separation; separation in TEN (toxic epidermal necrolysis) occurs at the dermal-epidermal junction

137
Q

What is Verruca?

A

(wart) Flesh-colored papules with a rough surface

138
Q

What is verruca due to?

A

HPV infection of keratinocytes;

139
Q

What is Verruca characterized by?

A

koilocytic change

140
Q

What are common locations for verruca?

A

Hands and feet

141
Q

What is molluscum contagiosum?

A

Firm, pink, umbilicated papules due to poxvirus;

142
Q

In molluscum contagiosum, what happens to the affected keratinocytes?

A

it shows cytoplasmic inclusions (molluscum bodies)

143
Q

In whom does molluscum contagiosum most often arise? Who else does it arise?

A

in children; also occur in sexually active adults and immunocompromised individuals

GBA Pathology (20 decks)

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