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My Pathoma Unit 2 > Chapter 19 Skin Pathology > Flashcards

Chapter 19 Skin Pathology Flashcards

1
Q

What are the four layers of the epidermis?

A

Stratum Basalis - regenerative (Stem cell) layer
Stratum Spinosum - Characterized by desmosomes between keratinocytes
Stratum Granulosum - Characterized by granules in keratinocytes
Stratum Corneum - characterized by keratin in anucleate cells

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2
Q

What does the dermis consist of?

A

Connective tissue, nerve endings, blood and lymphatic vessels, and adnexal structures (Hair shafts, sweat glands, sebaceous glands)

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3
Q

How does Atopic (Eczematous) Dermatitis present?

A

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

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4
Q

What causes Atopic (Eczematous) Dermatitis?

A

Type I hypersensitivity reaction; associated with asthma and allergic rhinitis

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5
Q

How does contact dermatitis present?

A

Pruritic, erythematous, oozing rash with vesicles and edema

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6
Q

What can cause contact dermatitis?

A

exposure to allergens such as:
1 poison ivy and nickel jewlery (type 4 hypersensitivity)
2 irritant chemicals (Detergents)
3 Drugs (penicillin)

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7
Q

What is the treatment for contact dermatitis and Atopic dermatitis?

A

Removal of offending agent and topical glucocorticoids if needed

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8
Q

How does acne vulgaris present?

A

Comedones (whiteheads and blackheads), pustules (pimples), and nodules

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9
Q

What causes acne vulgaris?

A

chronic inflammation of hair follicles and associated sebaceous glands.
-Hormone associated increase in sebum production (sebaceous glands have androgen receptors) and excess keratin production block follicles, forming comedones

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10
Q

What organism infects acne vulgaris and what effects does it have?

A

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

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11
Q

What does treatment for acne vulgaris include?

A

Benzoyl peroxide (antimicrobial) and vitamin A derivatives which reduce keratin formation

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12
Q

How does psoriasis present?

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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13
Q

What causes psoriasis?

A

Excessive keratinocyte proliferation

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14
Q

What is the etiology of psoriasis?

A

Possible autoimmune associated with HLA-C

lesions often arise in areas of trauma (environmental trigger)

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15
Q

What histological features are seen in psoriasis?

A

Acanthosis (epidermal hyperplasia)
Parakeratosis (Hyperkeratosis with retention of keratinocyte nuclei in the stratum corneum)
Collections of neutrophils in the stratum corneum (Munro microabscesses)
Thinning of the epidermis aboce elongates dermal papillae; results in pinpoint bleeds when scale is picked off (Auspitz sign)

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16
Q

What does treatment of psoriasis involve?

A

Corticosteroids (autoimmune etiology)
UV-A light (Damage proliferating keratinocytes)
Psoralen (increases UVA absorption)
immune modulating therapy

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17
Q

How does lichen Planus present? Appearance and locations

A

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

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18
Q

What does histology show in lichen planus?

A

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

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19
Q

What is the etiology of Lichen planus?

A

Etiology is unknown; associated with chronic HCV infection

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20
Q

What causes Pemphigus vulgaris?

A

Autoimmune destruction of desmosomes between keratinocytes, due to IgG antibody against desmoglein (type II hypersensitivity)

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21
Q

How does pemphigus vulgaris present? 4 facts (gross and microscopic)

A

Skin and oral mucosa bullae
1 Acantholysis (seperation) of stratum spinosum keratinocytes (normally connected by desmosomes) results in suprabasal blisters
2 Basal layer cells remain attached via hemidesmosomes and looks like tomb stones
3 Thin walled bullae rupture easily (nikolsky sign), leading to shallow erosions with dried crust
4 immunoflorescence highlights IgG surrounding keratinocytes in a ‘fish net’ pattern

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22
Q

What causes bullous pemphigoid?

A

autoimmune destruction of hemidesmosomes between basal cells and the underlying basement membrane. Due to IgG antibody against hemidesmosome componenets (BP180) of the basement membrane

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23
Q

How does Bullous pemphigoid present?

A

blisters of the skin, usually in the elderly; oral mucosa is spared
1 basal cell layer is detached from the BM
2 tense bullae do not rupture easily; clinically milder than pemphigus vulgaris

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24
Q

What does immunfluorescence show in bullous pemphigoid?

A

highlights IgG along basement membrane (linear pattern)

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25
Q

What causes Dermatitis herpetiformis?

A

Autoimmune deposition of IgA at the tips of the dermal papillae

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26
Q

How does Dermatitis herpetiformis present?

A

pruritic vesicles and bullae that are grouped

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27
Q

What other disease is dermatitis herpetiformis associated with and how does this effect treatment?

A

Celiac disease. The IgAs are against gluten and cross react with reticulin fibers that attach the BM to the Dermis. If you go on gluten free diet it will resolve

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28
Q

what causes erythema multiforme and what does it look like?

A

Hypersensitivity reaction characterized by targetoid rash and bullae. Targetoid appearance is due to central epidermal necrosis surrounded by erythema.

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29
Q

What infection is erythema multiforme most commonly associated with? what others?

A

HSV.

others include mycoplasma infection, drugs (penicillin and sulfonamides), autoimmune disease (SLE) and malignancy

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30
Q

What is Stevens-Johnson Syndrome?

A

Erythema Multiforme with oral mucosa/lip involvement and fever

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31
Q

What is Toxic Epidermal necrolysis? what is it most often caused by?

A

Severe form of SJS characterized by diffuse sloughing of skin, resembling a large burn; most often due to adverse drug reaction

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32
Q

What is seborrheic keratosis?

A

Benign squamous proliferation; common tumor in the elderly

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33
Q

How does seborrheic keratosis present?

A

raised, discolored plaques on the extremities or face; often has a coin-like, waxy, ‘stuck-on’ appearance

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34
Q

What is seborrheic keratosis represented by histologically?

A

keratin pseudocysts

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35
Q

What is a Leser-Trelat sign? what does it suggest?

A

Sudden onset of multiple seborrheic keratoses and suggest underlying carcinoma of the GI tract

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36
Q

What is Acanthosis nigricans?

A

Epidermal hyperplasia with darkening of the skin often involving the axilla or groin

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37
Q

What is acanthosis nigricans associated with?

A

insulin resistance (type II diabetes) or malignancy (especially gastric carcinoma)

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38
Q

What is basal cell carcinoma?

A

Malignant proliferation of the basal cells of the epidermis

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39
Q

What are the risk factors for basal cell carcinoma?

A

UVB induced DNA damage, prolonged exposure to sunlight, albinism, and xeroderma pigmentosum

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40
Q

How does basal cell carcinoma present?

A

elevated nodule with a central, ulcerated crater surrounded by dilated (telangiectatic) vessels “Pink, pearl like papule”
Classic location is upper lip

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41
Q

What does histology show in basal cell carcinoma?

A

nodules of basal cells with peripheral palisading

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42
Q

What is the treatment and prognosis for basal cell carcinoma?

A

Treatment is surgical excision; metastasis is rare and outlook is good

43
Q

What is squamous cell carcinoma?

A

Malignant proliferation of squamous cells characterized by the formation of keratin pearls

44
Q

What are the risk factors for squamous cell carcinoma? There are additional risk factors on this card.

A

Stem from UVB induced damage to DNA, include prolonged exposure to sun, albinism, and xeroderma pigmentosum

Additional factors include immunosuppresice therapy, arsenic exposure, and chronic inflammation (scar from burn or draining sinus tract)

45
Q

How does squamous cell carcinoma present?

A

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

46
Q

What is the treatment for squamous cell carcinoma? what is the prognosis?

A

excision; metastasis is rare and prognosis is good

47
Q

What is a precursor lesion for squamous cell carcinoma?

A

Actinic keratosis

48
Q

how does actinic keratosis present?

A

hyperkeratotic, scaly plaque, often on the face, back or neck

49
Q

What is a Keratoacanthoma? how does it present?

A

Well differentiated squamous cell carcinoma that develops rapidly and regresses spontaneously; presents as a cup-shaped tumor filled with keratin debris.

50
Q

Where are melanocytes located?

A

in the basal layer of the epidermis

51
Q

Where are melanocytes derived from?

A

neural crest cells

52
Q

What is the purpose of melanocytes?

A

synthesize melanin in melanosomes using tyrosine as a precursor molecule

53
Q

How do keratinocytes become pigmented?

A

Melanocytes pass melanosomes

54
Q

What is Vitiligo?

A

localized loss of skin pigmentation due to autoimmune destruction of melanocytes

55
Q

What causes albinism and what is it?

A

Congenital lack of pigmentation due to enzyme defect (usually tyrosinase) that impairs melanin production

56
Q

What are the two forms or albinism?

A 
ocular form (just eyes)
oculocutaneous form (both skin and eyes)
57
Q

What does albinism cause an increased risk for?

A

squamous cell carcinoma, basal cell carcinoma, melanoma due to reduced protection against UVB

58
Q

What is a freckle (Ephelis)

A

Small tan to brown macule; darkens when exposed to light due to increased number of melanosomes (melanocytes are not increased)

59
Q

What is melasma? what is it associated with?

A

Mask-like hyperpigmentation of the cheeks associated with pregnancy and oral contraceptive

60
Q

What is a nevus (mole)?

A

A benign neoplasm of melanocytes

61
Q

How can you differentiate a congential nevus from an acquired one?

A

Congenital will have hair

62
Q

What is the progression of a nevus?

A

1 begins as nests of melanocytes at the dermal-epidermal junction (junctional nevus); most common in children
2 Grows by extension into the dermis (Compound nevus)
3 Junctional component is eventually lost resulting in an intradermal nevus, which is the most common mole in adults

63
Q

What does a mole look like?

A

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

64
Q

What is a melanoma?

A

malignant neoplasm of melanocytes

65
Q

What are the risk factors for melanoma?

A

Exposure to sunlight, albinism, xeroderma pigmentosum and dysplastic nevus syndrome

66
Q

What is dysplastic nevus syndrome?

A

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

67
Q

What is the ABCD scale for melanoma?

A

Asymmetry
Borders are irregular
Color is not uniform
Diameter is >6mm

68
Q

What are the two growth phases of melanoma?

A

1 Radial growth horizontally along the epidermis and superficial dermis; low risk of metastasis
2 Vertical growth into the deep dermis
- increased risk for metastasis;

69
Q

What is the most important prognostic factor in predicting metastasis of a melanoma?

A

The breslow thickness which is the depth of extension

70
Q

What are the 4 variants of melanoma?

A

1 superficial spreading - most common subtype; dominant early radial growth results in good prognosis
2 Lentigo maligna melanoma - lentiginous (along dermal epidermal jn) ; good prognosis
3 Nodular - early vertical growth; poor prognosis
4 Acral lentiginous - arises on palms or soles, often in dark skinned individuals; not related to UV light exposure

71
Q

What is Impetigo?

A

superficial bacterial skin infection, most often due to S aureus or S pyogenes

72
Q

How does impetigo present?

A

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

73
Q

What is cellulitis?

A

Deeper (dermal and subcutaneous) infection usually due to S aureus or S pyogenes

74
Q

How does cellulitis present?

A

red, tender, swollen rash with fever

75
Q

What are risk factors for cellulitis?

A

recent surgery, trauma, or insect bite

76
Q

What can cellulitis progress to that is much more aggressive?

A

Necrotizing fasciitis with necrosis of subcutaneous tissues due to infection with anaerobic ‘flesh-eating’ bacteria
1 production of CO2 lead to crepitus
2 surgical emergency

77
Q

What is staphylococcal scalded skin syndrome?

A

sloughing of skin with erythematous rash and fever; leads to significant skin loss. due to S aureus infection; exfoliative A and B toxins results in epidermolysis of the stratum granulosum

78
Q

How is staphyloccocal scalded skin syndrome distinguished histologically from toxic epidermal necrolysis?

A

by the level of skin seperation; seperation in TEN occurs ar the dermal-epidermal junction which is much deeper

79
Q

What is a Verruca (wart) presentation, cause, locations

A

Flesh colored papules with a rough surface due to HPV infection of keratinocytes; characterized by koilocytic change. hands and feet are common locations.

80
Q

What is Molluscum Contagiosum?

A

Firm, pink, umbilicated papules due to poxvirus; affected keratinocytes show cytoplasmic inclusions (molluscum bodies)

81
Q

What demographic does molluscum contagiosum affect?

A

Most often arise in children; also occur in sexually active adults and immunocompromised individuals

82
Q

What cytokines make up the cytokine soup in psoriasis?

A

IL-12, INF gamma, TNF, IL 17

83
Q

What two cells are associated with the inflammation of lichen planus?

A

CD8+ Tcells and langerhans cells

84
Q

Describe the distribution of CD 4 and 8 Tcells in erythema multiforme?

A

CD8 are prominent in the center and CD4 on the periphery.

85
Q

What is a common activating mutation in seborrheic keratosis?

A

Fibroblast growth factor receptor 3 (FGFR3)

86
Q

Is there melanocytic hyperplasia in acanthosis nigricans?

A

No

87
Q

Describe the etiology of familial and Type II diabetes related acanthosis nigricans?

A

Familial- FGFR3 mutation

Type II diabetes - upreg of insulin like growth factor receptor 1 which has same downstream path as FGFR3

88
Q

What mutations lead to basal cell carcinoma?

A

Mutations that upregulate SHH signaling. LOF in PTCH causes constitutive SMO signaling which increases transcription of GL1

89
Q

epidermodysplasia verrucaformis causes a high susceptibility for what?

A

squamous cell carcinoma

90
Q

What HPV strains is squamous cell carcinoma associated with?

A

mainly 5 and 8

91
Q

What is the main mutation seen in squamous cell carcinomas?

A

P53

Ras and Notch to a lesser extent

92
Q

What two mutations are common in nevi?

A

Mutations in either RAS or BRAF

93
Q

Why do most Nevi never progress to melanoma?

A

Protective function of p16/INK4a inhibits CDK 4 and 6

94
Q

What are some morphological changes seen in moles?

A

Deeper cells are smaller and produce little to no melanin, appears as chords and single cells. At deepest extent, cells acquire fusiform contours and grow in fascicles resembling neural tissue

95
Q

What is the morphology of melanoma cells?

A

unlike melanocytic nevi, “neurotization” is absent. Individual cells are considerably larger than normal melanocytes

96
Q

What is a common mutation seen in dysplastic nevi or melanoma?

A

CDKN2A causes loss of p16/INK4a protective function and leads to progression

97
Q

Does melanoma incite a host immune response?

A

Yes, often

98
Q

What gene involving telomerase is mutated in many melanomas?

A

TERT - reactivates telomerase

99
Q

What is a melanocyte cell marker?

A

HMB-45

100
Q

What does S. aureus toxin cleave in impetigo?

A

desmoglein 1

101
Q

Describe the effects of the E6 protein in HPV 5 and 8 and how it differs from the high risk strains

A

The E6 in 5 and 8 does not affect P53 and has low oncogenic potential

102
Q

What HPV strains are associated with anogenital warts?

A

6 and 11

103
Q

are mulluscum bodies eosinophilic or basophilic

A

eosinophillic

My Pathoma Unit 2 (6 decks)

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