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(J2) Skin > Inflammatory Lesions > Flashcards

Inflammatory Lesions Flashcards

1
Q

What is ichthyosis?

(appearance and histologic features)

A

impaired epidermal maturation

  • hyperkeratosis
  • dry, coarse “fish-like” scales
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2
Q

Where and in what populations is ichthyosis most commonly seen?

A

-extensor surfaces

Inherited: first year of life, usually resolving around adolescence

Aquired: as a paraneoplastic syndrome

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3
Q

What is urticaria?

(appearance and histologic features)

A

hives/wheals

  • transient, pruitic, edmatous papules/plaques
  • angioedema: swelling of dermis and subcutaneous fat
  • dermal edema
  • epidermis unchanged
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4
Q

What are the mechanisms of urticaria?

A

Mast cell degranulation:

  • IgE dependent; type I hypersensitivities/allergies/anaphylaxis
  • IgE independent; substances that stimulate degranulation directly
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5
Q

What is acute eczematous dermatitis?

(appearance and histologic features)

A
  • red papular/vesicular, oozing, crusted lesions
  • scaling plaques if persistent

Acute lesions

  • spongiosis (edema of the epidermis)
  • acantholysis (seperation of keratinocyte -> vesicle formation)

Persistent lesions

  • acanthosis (diffuse epidermal hyperplasia)
  • hyperkeratosis
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6
Q

What is the mechanism of acute eczematous dermatitis?

A

Type IV hypersensitivity

-requires sensitization

-delayed reaction following stimulus

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7
Q

What is erythema multiforme?

(appearance and histologic features)

A

self-limited T-cell mediated, hypersensitivity

  • various lesions types (hence multiforme), classically erythematous macule -> papule -> targetoid lesion
  • infiltrating lymphocytes
  • areas of epidermal necrosis
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8
Q

Where and in what populations is erythema multiforme most commonly seen?

A
  • typically start on hands/feet and extend proximally
  • young/middle aged adults (20-40 years)
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9
Q

What are common causes of erythema multiforme?

A

Infection

  • herpes simpex
  • mycoplasma
  • histoplasmosis
  • coccidiodomycosis
  • typhoid

Drugs:

  • penicillins
  • sulfonamides
  • antimalarials

Certain cancers

Autoimmune diseases

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10
Q

What is Stevens-Johnson syndrome?

A

Complication of erythema multiforme

  • targetoid lesions of erythema multiforme
  • fever*** (differentiating feature)
  • involvement of <10% surface area
  • involvement of mucous membranes
  • sloughing of skin -> fluid loss -> shock
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11
Q

What is toxic epidermal necrolyis (TEN)?

A

Severe form of Stevens-Johnson syndrome

  • fever
  • targetoid lesions of erythema multiforme
  • involvement of >30% surface area*** (differentiating feature)
  • involvement of mucous membranes
  • sloughing of skin -> fluid loss -> shock
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12
Q

What is psoriasis?

(appearance and histologic features)

A

Chronic inflammatory dermatosis

  • associated with mild to severly deforming arthritis
  • pink to salmon-colored plaque with adherent silver-white scale
  • pruritic
  • nail involvement (pitting or separation/onycholysis)
  • acanthosis (epidermal hyperplasia)
  • elognated rete ridges
  • Munro microabscesses (neutrophils in stratum conreum)
  • parakaratosis
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13
Q

Where and in what populations is psoriasis most commonly seen?

A
  • extensor surfaces
  • young/middle aged adults (20-40 years)
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14
Q

What are characteristic/diagnositic features of psoriasis?

A

Koebner phenomenon:

  • physical stimuli (scratching, irritation, or trauma) produces lesion
  • lesions are pruritic which can cause propagation of lesions

Auspitz sign:

-removal of scale results in pinpoint bleeding

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15
Q

What is the treatment for psoriasis?

A

-corticosteroids

PUVA

-Psoralen with UVA

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16
Q

What is seborrheic dermatitis?

(appearance and histologic features)

A

Chronic inflammatory dermatosis

  • dandruff is a form
  • erythematous papules on erythematous base with scales and greasy yellow crusts

-parakaratotic mounds

-follicular lipping

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17
Q

Where and in what populations is seborrheic dermatitis most commonly seen?

A

Oily skin (numerous sebaceous glands)

  • forehead, around the ears, nasolabial fold, presternal
  • more common in men (androgens?)
  • bimodal; infants and puberty
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18
Q

What conditions are associated with development of seborrheic dermatitis?

A
  • Malassezia colonization
  • adrongens (increased sebum)
  • Parkinson’s disease
  • HIV w/ low CD4 count
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19
Q

What is lichen planus?

(appearance and histologic features)

A

Chronic inflammatory dermatosis

six “P’s”

  • pruritic
  • purple
  • polygonal
  • planar (flat top)
  • papules
  • plaques

Wickham striae: white lines on surface of lesion

  • hyperkeratosis
  • hypergranulosis (-> Wickham striae)
  • saw-tooth acanthosis
  • band-like lymphocyte infiltrate of dermal-epidermal junction
20
Q

Where is lichen planus most commonly seen?

A

Symmetrically on extremities

-wrists, elbows, and ankles

Mucosa

21
Q

What condition is associated with development of lichen planus?

A

chronic hepatitis C infections

22
Q

What cancer is associated with lichen planus?

A

squamous cell carcinoma of chronically infected mucosa

23
Q

What is pemphigus?

(mechanism, appearance, and histologic/immunofluorescence features)

A

Blistering disease

  • IgG autoantibodies against desmogleins (in desmosomes)
  • vesicles/bullae -> rupture to form erosions and crusts
  • non-pruritic
  • acantholysis (above the basal layer)
  • “tombstone” appearance; basal layer attached to basement membrane
  • fishnet-like immunofluorescence surrounding keratinocytes
24
Q

Where and in what populations is pemphigus most commonly seen?

A
  • older adults (40-60)
  • first appear in oral mucosa, later in intertriginous areas
25
Q

What is a characteristic clinical finding of pemphigus that helps to differentiate it from other blister disorders?

A

Nikolsky’s sign:

-thin vesicle/bullae (they are intraepidermal and more superficial) readily rupture -> erosions and crusts

26
Q

What is bullous pemphigoid?

(mechanism, appearance, and histologic/immunofluorescence features)

A

Blistering disease

  • IgG autoantibodies against BPAg (in hemidesmosomes)
  • tense bullae, don’t rupture
  • pruritic

-subepidermal, nonakantholytic

-linear immunofluorescence along basement membrane

27
Q

Where and in what populations is bullous pemphigoid most commonly seen?

A
  • inner thigh, flexor surfaces, axilla, groin
  • RARE mucosal involvement
  • elderly (over 60)
28
Q

What is dermatitis herpetiformis?

(mechanism, appearance, and histologic/immunofluorescence features)

A

Blistering disease

  • IgA autoantibodies against gluten analog in epidermal basement membrane
  • tense, grouped vesicles (herpetiform)
  • extremely pruritic
  • subepidermal blister at tip of dermal papillae

-noncontinuous immunofluorescence at tip of dermal papillae

29
Q

Where and in what populations is dermatitis herpetiformis most commonly seen?

A
  • extensor surfaces
  • NO mucosal involvement
  • middle aged adult males (30-40)
30
Q

What condition is associated with development of dermatitis herpetiformis?

A

celiac disease, autoantibody is against gluten like substance in basement membrane

31
Q

What is the treatment for dermatitis herpetiformis?

A

gluten free diet

32
Q

What is epidermolysis bullosa?

(mechanism and onset)

A

Non-inflammatory, inherited blistering disease

  • blisters easily form from mechanical stress
  • onset at birth
33
Q

What are porphyrias and how do they relate to the skin?

(mechanism)

A

Inherited defects in porphyrin synthesis

  • deposition of intermediates into skin can occur -> fragile skin -> blisters
  • subepidermal vesicles, scar when ruptured
  • worsens with sun exposure
34
Q

What is acne vulgaris?

(appearance and histologic features)

A
  • erythematous papules, nodules, or pustules
  • may have open or closed comedones, white/black heads (keratin plug either visible or below epidermal surface)
35
Q

What are causes of acne vulgaris?

A
  • keratinization of follicle -> keratin plug
  • hypertrophy of sebaceous glands (androgens in puberty)
  • Propionibacterium acnes colonization of follicle
36
Q

What is the treatment for acne vulgaris?

A
  • benzoyl peroxide (antimicrobial)/antibiotics
  • vitamin A derivatives
37
Q

What is rosacea?

(appearance and histologic features)

A
  • facial flushing
  • persistent erythema w/ telangiectasia
  • pustules/papules
  • rhinophyma (thickend nasal skin by papules)
38
Q

What is the mechanism of rosacea?

A

-increased levels of cathelicidin (antimicrobial peptides)

39
Q

Where and in what populations is rosacea most commonly seen?

A
  • face, particularly around the nose
  • more common in women
  • mid-older adults (30-60)
40
Q

What is paniculitis?

A

inflammation of subcutaneous adipose

41
Q

What is erythema nodosum?

(appearance and histologic features)

A

Panniculitis (subcutaneous adipose inflammation)

  • firm, tender, erythematous nodules
  • more noticeable by palpation than inspection
  • subcutaneous edema and infiltration
42
Q

What is erythema induratum?

(appearance and histologic features)

A

Panniculitis (subcutaneous adipose inflammation)

  • tender, erythematous nodules
  • ulcerate
  • subcutaneous granulomas/necrosis
43
Q

What are verrucae?

(appearance and histologic features)

A

Warts (HPV infection)

  • skin colored papules
  • epidermal hyperkeratosis/hyperplasia
44
Q

What is molluscum contagiosum?

(appearance and histologic features)

A

caused by Pox virus

  • skin colored papule with umbilication
  • Molluscum bodies
45
Q

What is impetigo?

(appearance and histologic features)

A

Staphylococcus aureus (bullous) or Strep A (non-bullous) infection of the skin

  • erythematous macules -> pustules
  • honey-colored crust
  • neutrophil infiltration under stratum corneum -> pustules

(J2) Skin (7 decks)

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