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MSS > Skin Pathology (Non-pigmented Lesions) > Flashcards

Skin Pathology (Non-pigmented Lesions) Flashcards

1
Q

What is the skin?

A
  • a barrier against environmental insults and fluid loss.
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2
Q

What are the 2 main layers of the skin?

A
  1. epidermis = keratinocytes
  2. dermis= connective tissue, nerve endings, blood vessels, lymphatic vessels, and adnexal structures (hair shafts, sweat glands, and sebaceous glands).
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3
Q

What are the 4 layers of the epidermis?

A
  1. Stratum basalis
  2. Stratum spinosum
  3. Stratum granulosum
  4. Stratum corneum
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4
Q

What layer of the epidermis is the regenerative stem cell layer?

A
  • Stratum BASILIS
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5
Q

What characterizes the stratum spinosum?

A
  • DESMOSOMES between keratinocytes
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6
Q

What characterizes the stratum GRANULOSUM?

A
  • granules in keratinocytes
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7
Q

What characterizes the stratum corneum?

A
  • keratin in ANUCLEATE cells.
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8
Q

What is Atopic Dermatitis (Eczema)?

A
  • pruritic, erythematous, oozing rash with vesicles and edema; often involves the face and flexor surfaces.
  • TYPE I hypersensitivity reaction associated with asthma and allergic rhinitis.
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9
Q

What is Contact Dermatitis?

A
  • pruritic, erythematous, oozing rash with vesicles and edema that arises upon exposure to ALLERGENS.
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10
Q

What allergens commonly cause contact dermatitis?

A
  • poison ivy and nickel jewelry= TYPE IV hypersensitivity.
  • irritant chemicals (ex. detergents).
  • drugs (ex. penicillin)
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11
Q

How do you treat contact dermatitis?

A
  • remove the offending agent and topical glucocorticoids.
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12
Q

What is Acne Vulgaris?

A
  • comedomes (whiteheads and blackheads), pustules (pimples), and nodules (from scarring) due to chronic inflammation of hair follicles and associated sebaceous glands.
  • extremely common, especially in adolescents.
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13
Q

What is the pathogenesis of acne vulgaris?

A
  • hormone-related increase in sebum production (sebaceous glands have androgen receptors) and excess keratin production block follicles, forming comedomes.
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14
Q

What bacteria causes acne vulgaris?

A
  • PROPIONIBACTERIUM ACNES, which produces LIPASES that break down sebum, releasing proinflammatory fatty acids, which results in pustule or nodule formation.
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15
Q

How do you treat acne vulgaris?

A
  • benzyol peroxide (antimicrobial).

- vitamin A derivatives (isotretinoin), which reduces keratin production.

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16
Q

*** What is Psoriasis?

A
  • well-circumscribed salmon-colored plaques with SILVERY SCALE, due to excessive keratin proliferation (possibly autoimmune).
  • usually on extensor surfaces and scalp.
  • may see pitting of nails.
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17
Q

With what is psoriasis associated?

A
  • HLA-C

- areas of trauma (environmental triggers).

18
Q

*** What histology will you see with psoriasis?

A
  • ACANTHOSIS (epidermal hyperplasia)
  • PARAKERATOSIS (hyperkeratosis with retention of keratinocyte nuclei in the stratum corneum).
  • collections of neutrophils in the stratum corneum (MUNRO ABSCESSES).
  • thinning of the epidermis above elongated dermal papillae; results in bleeding when scale is picked off (AUSPITZ SIGN).
19
Q

How do you treat psoriasis?

A
  • corticosteroids
  • UV light with psoralen
  • immune modulating therapy
20
Q

** What is Lichen Planus? (5 Ps)

A
  • Pruritic, Planar, Polygonal, Purple Papules, often with reticular white lines on surface (WICKHAM STRIAE).
  • commonly involves wrists, elbows, and oral mucosa.
21
Q

*** What histology will you see with lichen planus?

A
  • inflammation of the dermal-epidermal junction with a SAW-TOOTH appearance.
22
Q

With what is lichen planus associated?

A
  • chronic hepatitis C virus
23
Q

What is a blister?

A
  • space or bubble within the skin
24
Q

What is Pemphigus Vulgaris?

A
  • autoimmune destruction of desmosomes (Dsg1 and Dsg3) between keratinocytes due to IgG antibody against DESMOGLEIN (TYPE II hypersensitivity).
  • often seen in areas where skin rubs against skin.
25
Q

How does Pemphigus Vulgaris present?

A

As SKIN and ORAL bullae (blister):

  • ACANTHOLYSIS (separation) of the stratum spinosum keratinocytes (normally connected by desmosomes) results in SUPRAbasal blisters.
  • basal layer cells remain attached to basement membrane via hemidesmosomes (TOMBSTONE appearance).
  • thin-walled bullae rupture easily (NIKOLSKY SIGN), leading to shallow erosions with dried crust.
26
Q

What will immunofluorescence show in pemphigus vulgaris?

A
  • IgG surrounding keratinocytes in a FISH NET pattern.
27
Q

*** What is Bullous Pemphigoid?

A
  • autoimmune (IgG antibody) destruction of hemidesmosomes (BP180) between basal cells and the underlying basement membrane; where bullous pemphigoid antigen 2 (BPAG2) is located.
28
Q

How does bullous pemphigoid present?

A
  • as SUB-EPIDERMAL blisters of the skin, usually in the elderly.
  • tense bullae do not rupture easily.
  • oral mucosa is SPARED.
29
Q

What will immunofluorescence show in bullous pemphigoid?

A
  • IgG along basement membrane (LINEAR pattern).
30
Q

** What is Dermatitis Herpetiformis?

A
  • autoimmune deposition of IgA at the tips of dermal papillae.
  • strong association with CELIAC DISEASE and resolves with gluten-free diet.
31
Q

*** How does Dermatitis Herpetiformis present?

A
  • as pruritic vesicles and bullae that are grouped (herpetiform).
32
Q

** What is Erythema Multiforme?

A
  • hypersensitivity reaction characterized by TARGETOID RASH (due to central epidermal necrosis surrounded by erythema) and bullae.
  • Most commonly associated with HERPES SIMPLEX VIRUS infection
33
Q

** Besides HSV, with what else is erythema multiforme associated?

A
  • Mycoplasma, drugs (penicillin and sulfonamides), autoimmune disease (SLE) and malignancy.
34
Q

*** What is erythema muliforme with oral mucosa/lip involvement and fever termed?

A
  • Stevens-Johnson syndrome (SJS)
35
Q

*** What is toxic epidermal necrolysis (TEN)?

A
  • a severe form of SJS characterized by diffuse sloughing of skin, resembling a large burn
  • most often due to an adverse drug reaction
36
Q

What is Pemphigus vegetans?

A
  • rare, large, moist, verucous plaques.
  • pustules also present on the goirn, axillae, adn flexural surfaces.
  • Acantholysis (cells above the basal cell layer)
37
Q

What is Pemphigus foliaceus?

A
  • more benign form of pemphigus, endemic to Brazil.
  • involves scalp, face, chest, and back
  • no mucous membrane involvement.
  • acantholysis forms a LEAF-LIKE blister in the superficial epidermis because the autoantibodies are directed against the DSG1 ALONE.
38
Q

What is Pemphigus erythematosus?

A
  • localized less severe form of pemphigus foliaceus.

- may selectively involve the MALAR AREA of the FACE in a LUPUS LIKE fashion.

39
Q

What is Paraneoplastic pemphigus?

A
  • occurs in association with lymphoid malignancies.
  • most common is NON-HODGKIN LYMPHOMA
  • caused by autoantibodies that recognize desmogleins.
40
Q

What is Epidermolysis bullosa?

A
  • inherited defects in structural proteins that give stability to the skin.
  • tend to form blisters at sites of rubbing, pressure, or trauma.
41
Q

What are the 3 types of Epidermolysis bullosa?

A
  1. Simplex= defects in basal cell layer from mutations in genes encoding KERATIN 14 and 15.
  2. Junctional= blisters occur in otherwise normal skin at the level of the LAMINA DENSA.
  3. Dystrophic= blisters develop under the lamina densa resulting from mutations in the COL7A1 gene, which encodes for type VII collagen.
42
Q

What is Porphyria?

A
  • inborn or acquired disturbances in porphyrin metabolism (pigments present in hemoglobin, myoglobin, and cytochromes).
  • leads to urticaria, SUBepidermal vesicles that heal with scarring, and are EXACERBATED by SUNLIGHT.

MSS (9 decks)

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