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MSK II Midterm > Skin Pathology > Flashcards

Skin Pathology Flashcards

1
Q

Actopic Dermatitis (eczema)

A
  • pruritic, erythematous, oozing rash with vescicles and edema, often involved face and flexor surfaces
  • Type 1 hypersensitivity
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2
Q

Contact dermatitis

A
  • pruritic, erythematous, oozing rash with vesicles and edema
  • arises upone exposure to allergens like poison ivy and whatnot
  • tx involves removal of the ffending agent and topical glucocorticoids, if needed
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3
Q

Acne vulgaris

A
  • Comedones (black and white heads), pustules (pimples), and nodules
  • chronic inflammation of hair follicles and associated sebaceous glands
  • increase in sebum production
  • propionibacterium acnes infection… FA’s released, results in pustule or nodule formation
  • Tx includes benzoyl peroxide and Vit A derivatives, which reduce keratin production
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4
Q

Psoriasis

A
  • well-circumscribed, salmon colored plaques with silvery scale, usually on extensor surfaces and scalp, pitting of nails may also be present
  • due to excessive keratinocyte proliferation
  • autoimmune, HLA-C
  • Lesions in areas of trauma
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5
Q

Histology of psoriasis?

A
  • acanthosis
  • parakeratosis
  • collections of neutrophils in the stratum corneum (munro microabscesses)
  • thinning of epidermis above elongated dermal papillae… results in bleeding when scale is picked off (auspitz sign)
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6
Q

Tx for psoriasis

A

-corticosteroids, UV light with psoralen, or immune modulating therapy

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7
Q

Lichen Planus

A
  • The p disease
  • Pruritic, planar, polygonal, purple papules\, often with reticular white lines on their surface…. commonly involves wrists, elbows, and oral mucosa
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8
Q

What does the oral involvement of lichen planus manifest as?

A

-whickham striae

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9
Q

Histo for lichen planus

A

-inflammation of the derma epidermal junction with a “saw tooth” appearance

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10
Q

Pemphigus vulgaris

A
  • AI destruction of desmosomes b/w keratinocytes
  • IgG antibody against desmoglein (type 2 hypersensitivity)
  • Presents as skin and ORAL mucosa bullae
  • rupture easily… dried crust
  • IF highlights IgG surrounding keratinocytes in a “fish net” pattern
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11
Q

What gives pemhpigus vulgaris its tombstone appearance?

A

-basal layer cells remain attached to basement membrane via hemidesomosomes

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12
Q

Bullous Pemphigoid

A
  • AI destruction of hemidesmosomes betwen basal cells and the underlying basement membrane
  • IgG ab against hemidesmosome components(BP180) of basement membrane
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13
Q

Presentation of bullous pemphigoid

A
  • blisters of the skin, usually in the elderly
  • oral mucosa is spared
  • do NOT rupture easily… clinically milder than pemphigus vulgaris
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14
Q

What will IF staining look like in bullous pemphigoid?

A
  • highlights IgG along basememnt membrane (linear pattern)

- pemphigus vulgaris was a fish net

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15
Q

Dermatitis herpetiformis

A
  • AI deposition of IgA at the tips of dermal papillae
  • Presents as Pruritic vesicles and bullae that are grouped
  • strong association with celiac disease; resolves with gluten-free diet
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16
Q

Erythema multiforme (EM)

A
  • hypersensitivity rxn: targetoid rash and bullae: central epidermal necrosis surrounded by erythema
  • HSV infection
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17
Q

What is it called if we see EM with oral mucosa/lip involvement and fever?

A
  • Stevens-Johnson syndrome (SJS)
  • toxic epidermal necrolysis, severe form of SJS with diffuse sloughing of skin… looks like large burn… adverse drug rxn
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18
Q

Seborrheic Keratosis

A

-Benign squamous proliferation; common tumor in the elderly

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19
Q

Seborrheic keratosis (SK) presentation

A
  • raise, discolored plaques on the extremities or face
  • often has a coin-like, waxy, stuck-on appearance
  • characterized by keratic pseudocysts on histology
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20
Q

What is Leser-Trelat sign?

A

-the sudden onset of multiple seborrheic keratoses and suggests underlying carcinoma of the GI tract

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21
Q

What mutation is associated with SK?

A

-FGFR3

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22
Q

Mutation for Paget’s?

A

-SQSTM1

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23
Q

Mutation for fibrous dysplasia

A

-GNAS1

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24
Q

What are Acrochondons?

A
  • neck and axilla
  • hormonally sensitive
  • Birt-Hogge-Dube syndrome
  • They’re freaking skin tags!!!!
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25
Q

What are eccrine poromas?

A

-on palms and soles

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26
Q

What is erythema nodosum?

A
  • B strep

- tender erythematous plaques…. poorly defined

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27
Q

Acanthosis Nigricans

A
  • epidermal hyperplasia with darkening of the skin… often involves the axilla or groin
  • associated with insulin resistance or malignancy (especially gastric carcinoma)
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28
Q

Basal Cell carcinoma

A
  • Malignant proliferation of the basal cells of the epidermis
  • most common cutaneous malignancy
  • risk factors stem from UVB-induced DNA damage and include prolonged exdposure to sunlight, albinism, and xeroderma pigmentosum
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29
Q

Presentation of BCC

A
  • elevated nodule with a central, ulcerated crater surrounded by dilated vessels
  • Pink, pearl like papule
  • classic location is the upper lip
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30
Q

Histology of BCC

A

-nodules of basal cells with peripheral palisading (means lining up against something)

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31
Q

Tx for BCC

A
  • surgical excision

- metastasis is rare

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32
Q

Squamous cell carcinoma

A
  • Malignant proliferation of squamous cells characterized by formation of keratin pearls
  • sun is risk factor
  • Immunosuppressive therapy can cause this as well
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33
Q

Presentation of SCC

A

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

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34
Q

Tx for SCC

A
  • excision

- mets are uncommon

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35
Q

What is actinic keratosis

A

-a precursor lesion of squamous cell carcinoma and presents as a hyperkeratotic, scaly plaque, often on the face, back, or neck

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36
Q

What is keratoacanthoma

A

-well differentiated SCC that develops rapidly and regresses spontaneously; presents as a cup-shaped tumor filled with keratin debris

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37
Q

What is the gene is wrong with BCC?

A

-PATCH abnormality

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38
Q

What syndrome is associated with BCC?

A

-Ghorlin syndrome

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39
Q

Mutation for dermato fibrosarcoma protuberans?

A
  • translocation involving PDGFB and COL1A1
  • increased secretion of PDFGB… drives tumor cell growth
  • “pinwheel” pattern= storiform
  • overlying dermis is generally thinned
40
Q

where are melanocytes?

A

-in the basal layer

41
Q

Where are melanocytes derived from?

A

-neural cerest

42
Q

Where is melanin made?

A

-in melanosomes

43
Q

Vitiligo

A

localized loss of skin pigmentation
-due to AI destruction of melanocytes
-

44
Q

Albinism

A
  • congenital lack of pigmentation
  • enzyme defect (tyrosinase) impairs melanin production
  • may involve the eyes or skin or both
  • increased risk of SCC, BCC, and melanoma due to reduced protection against UVB
45
Q

Freckle (Ephelis)

A
  • Small, tan to brown macule; darkens when exposed to sunlight
  • due to increased number of melanosomes
  • melanocytes are not increased***
46
Q

Melasma

A
  • Mask-like hyperpigmentation of the cheeks

- associated with pregnancy and oral contraceptives

47
Q

Nevus (mole)

A
  • benign neoplasm of melanocytes
  • congenital nevus is present at birth; often associated with HAIR
  • acquired nevus arises later in life
48
Q

Progression of an acquired nevus

A
  • beings as nests of melanocytes at the dermal-epidermal junction(junctional nevus); most common mole in children
  • grows by extension into the dermis (compound nevus)
  • junctional component by a flat macule or raised papule with symmetry, sharp borders, evenly distributed color, and small diameter (<6mm)
49
Q

What is a dysplastic nevus a precursor to?

A

-melanoma

50
Q

Mutation for Melanoma?

A

-CDKN2A

51
Q

Melanoma

A
  • malignant neoplasm of melanocytes; most common cause of death from skin cancer
  • risk facors from UVB
  • Presents as a mole-like growth wtih ABCD
52
Q

What does ABCD stand for?

A
  • asymmetry
  • borders are irregular
  • color is not uniform
  • diameter> 6mm
53
Q

What are the 2 growth phases for melanoma?

A
  • Radial growth…. horizantally along epidermis… low risk

- Vertical growth into deep dermis: increased risk

54
Q

What is the most important prognostic factor is predicting mets for Melanomas?

A

-depth of extension (breslow thickness)

55
Q

Superficial spreading melanoma

A
  • most common subtype
  • dominant early radial growth
  • results in good prognosis
56
Q

Lentigo maligna melanoma

A
  • lentiginous proliferation (radial growth); good prognosis
  • grows along ED junction
  • older men
57
Q

Nodular melanoma

A
  • early vertical growth

- poor prognosis

58
Q

Mutation for nodular melanoma

A

-HMB45

59
Q

Acral lentiginous melanoma

A
  • arises on the palms or soles, often in dark-skinned individuals
  • not related to UV light exposure***
60
Q

Impetigo

A
  • Superficial bacterial skin infection
  • staph Aureus
  • children
  • honey colored serum
  • histo: accumulation of neutrophils beneath the stratum corneum
  • bullous form in children
61
Q

Cellulitis

A
  • deeper infection, usually due to S aureus or S pyogenes
  • red, tender, swollen rash with fever
  • recent surgery, trauma, or insect bite are risk factors
  • can progress to neecrotizing fasciitis with necrosis of subcutaneous tissues due to infection with anaerobic “flesh -eating” bacteria
  • production of CO2 leads to crepitus
  • Surgical emergency if that happens
62
Q

Verruca (Wart)

A
  • flesh-colored papules with a rough surface
  • Due to HPV (11+16) infection of keratinocytes
  • koilocytic change
  • hands and feet are common locations
63
Q

Which HPV subtypes will give us SCC?

A
  • 5 and 8

- they produce variant E6 ptns that do not affect p53

64
Q

Molluscum contagiosum

A
  • poxvirus
  • dumbebell shaped DNA
  • Firm, pink, umbilicated papules due to poxvirus; affected keratinocytes show cytoplasmic inclusions on Geimsa stain (molluscum bodies)
  • Most often arise in children; also occur in sexually active adults and immunocompromised individuals
  • spread by direct contact
65
Q

Urticaria

A
  • localized mast cell degranulation
  • microvascular hyperpermeabiliy
  • produces prutitic edematous plaques called wheals
  • 20-40
66
Q

What does eczematous dermatitis typically result from?

A

-T cell-mediated inflammatory reactions (type 4 hypersensitivity)

67
Q

What cell is the problem in erythema multiforme?

A

-CD8+ T cells

68
Q

What will we see on histo for EM?

A

-accumulation of lymphocytes along the dermoepidermal junction

69
Q

What cell is the problem in ezcematous dermatitis?

A

-Langerhans cells… they are the ones that initiate the inflammatory response

70
Q

Which gene is associated with psoriasis?

A

HLA-C

-particularly: HLA-Cw*0602 allele

71
Q

is seborrheic dermatits a disease of the sebaceous glands?

A

-no, it’s the inflammation of the epidermis

72
Q

Common presentation for SD in the scalp?

A

-dandruff

73
Q

What is found at the ostia of hair follicles in Seborrheic dermatitis?

A

-mounds of parakeratosis containt neutrophils and serum (follicular lipping)

74
Q

What does lichen planus leave behind after it resolves?

A

-postinflammatory hyperpigmentation

75
Q

What is the Koebner phenomenon?

A

-when psoriatic lesions are induced in susceptible individuals by local trauma

76
Q

What other disease besides psoriasis does the Koebner phenomenon happen?

A
  • lichen planus

- remember, comes from local trauma

77
Q

What are Civatte bodies?

A
  • anucleate, necrotic basal cells that become incorporated into the inflamed papillary dermis
  • happens whenever basal keratinocytes are destroyed… but characteristic of lichen planus
78
Q

Pemphigus vegetans

A

-large, moist, verrucous, vegetating plaques studded with pustules on the groin, axillae, and flexural surfaces

79
Q

Pemphigous foliaceus

A
  • it’s in brazil
  • more superficial
  • erythema and crusting
  • mucous membranes rarely effected
80
Q

Pemphigus erythematosus

A
  • less intense than foliaceus

- malar area of the face in a lupus like fashion

81
Q

Paraneoplastic pemphigus

A

-occurs in association with various malignancies, most commonly non-hodgkin lymphoma

82
Q

What age ppl get bullous pemphigoids?

A

-older ppl

83
Q

Antibodies against what hemidesmosome component is present in bullous pemphigoid?

A

-BPAG2

84
Q

What disease will respond to a gluten free diet?

A
  • the one that is IgA related
  • Dermatitis herpetiformis
  • remember, this is the subepidermal blister
85
Q

Morphology of Dermatitis herpetiformis

A
  • lesions are b/l, symmetrical, and grouped
  • extensor surfaces
  • fibrin and neutrophils accumulate selectively at the tips of dermal papillae: microabscesses
  • IF will show discontinuous, granular deposits of IgA that selectively localize in the tips of the DERMAL PAPILLAE
86
Q

Epidermolysis bullosa

A
  • group of disorders caused bye inherited defects in structural ptns
  • common feature is proclivity to form blisters at sites of prssure, rubbing, or trauma, at or soon after birth
87
Q

In the most common type of epidermolysis bullosa, what is the mutations?

A
  • most common type is the simplex type

- mutations in genes encoding keratin 14 or 5

88
Q

Porphyria

A
  • group of uncommon inborn or acquired disturbances of porphyrin metabolism
  • scarring that is exacerbated by exposure to sunlight
  • subdermal vesicles
  • blood vessels have walls that are thickened by glassy deposits of serum proteins including Ig’s
89
Q

difference betwen open and closed comedones

A
  • open: small follicular papules containing a central black keratin plug… result of oxidation of melanin
  • Closed comedones: without a visible central plug… the keratin plug is trapped beneath the epidermal surface… these lesions are potential sources of follicular rupture and inflammation (these ones are identifiable only microscopically)
90
Q

Rosacea

A
  • cathelicidin is present, result of alternative processing by proteases such as kallikrein 5
  • rhinophyma is stage 4: permanent thickening of the nasal skin by confluent erythematous papules and prominent follicles
91
Q

Panniculitis

A
  • inflammatory rxn in the subcutaneous adipose tissue
  • erythema nodosum
  • erythema induratum
92
Q

Erythema nodosum

A
  • palpated, not seen
  • infections
  • poorly defined, exquisitely tender, erythematous plaques and nodules
93
Q

Erythema induratum

A
  • adolescents and menopausal women, uncommon
  • primary vasculitis of deep cessels
  • slightly tender nodule that usually goes on to ulcerate
  • usually no associated disease.. it just kinda happens
94
Q

factitial panniculitis

A

-caused by self-inflicted trauma or injection of foreign toxic substances

95
Q

Weber-Christian disease

A

-crops of erythematous plaques or nodules, predominantly on lower extremities

MSK II Midterm (15 decks)

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