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PATHOLOGY 2 > Skin > Flashcards

Skin Flashcards

1
Q
  1. Blistering skin disorders:

Pemphigus general information

A
  • rare autoimmune blistering disorder - loss of integrity of attachments between cells within epidermis and mucosal epithelium
  • autoimmune destruction of desmosomes
  • age: >50 years old
    TYPES:
    1. Pemphigus vulgaris
    2. Pemphigus foliaceus
    3. Paraneoplastic pemphigus
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2
Q
  1. Blistering skin disorders:

Pemphigus Pathogenesis

A
  • Type 2 hypersensitivity reaction + linkage to specific HLA types
  • IgG autoantibodies against intercellular desmosomal proteins (desmoglein 1 and 3)
    ⇒ anchoring between spinous cells lost ⇒ parts of skin “unzips” ⇒ fluid gathers ⇒ blister
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3
Q
  1. Blistering skin disorders:

Pemphigus Morphology

A
  1. PEMPHIGUS VULGARIS:
    - more in elderly + women
    - location: oral mucosa + skin (scalp, face, axilla, groin, trunk)
    - primary lesions: painful, superficial blisters - rupture easily
  2. PEMPHIGUS FOLIACEUS:
    - more rare and benign
    - location: skin
    - very superficial blisters ⇒ erythema and crusting sites
    - can be related to adverse drug reaction
    HISTOLOGY:
    - acantholysis
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4
Q
  1. Blistering skin disorders:

Bullous Pemphigoid

A

GENERAL:
- age: elderly
PATHOGENESIS:
- autoimmune disease ⇒ IgG AB and complement in sub epidermal zone
- IgG autoAB to hemidesmosomes(BPAG) ⇒ tissue injury
CLINICAL FEATURES:
- tense, nonacantholytic blisters filled with clear fluid
- blisters do not rupture; heal without scarring
- location: inner thigh, flexor surface, axilla, groin, lower abdomen

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5
Q
  1. Blistering skin disorders:

Dermatitis herpetiformis

A

GENERAL:
- rare disorder, urticaria + grouped vesicles
- more males, age 30-40
PATHOGENESIS:
- associated with celiac disease
- IgA AB against gluten ⇒ cross-react with reticulin ⇒ sub epidermal blister
MORPHOLOGY:
- urticarial plaques + vesicles pruritic
- lesions are bilateral, symmetrical + grouped
- location: extensor surface. elbow, knees, upper back, buttocks
HISTOLOGY:
- neutrophils in tips of dermal papillae ⇒ micro abscess
- basal cells show vacuolization + focal dermo-epidermal separation ⇒ blister

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6
Q
  1. Inflammatory skin diseases:

Urticaria Pathogenesis

A
  1. Antigen-induced release of vasoactive mediators from mast cell granules via sensitization with specific IgE AB (type 1 HR)
  2. IgE-independent urticaria: substances directly incite mast cell degranulation
  3. Hereditary angioedema: inherited deficiency of C1 esterase inhibitor ⇒ uncontrolled activation of complement
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7
Q
  1. Inflammatory skin diseases:

Urticaria Clinical feature

A
  • age: 20-40 years
  • individual lesion develop + fade within hours, episodes may persist days-months
  • lesions: small, itchy papules ⇒ large, edematous plaques
  • location: pressure points, trunk, distal extremities, ears
  • treatment: antihistamine, steroids
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8
Q
  1. Inflammatory skin diseases:

Acute Eczematous Dermatitis Types

A
  1. Allergic contact - topical exposure to allergen
  2. Atopic - defect in keratinocyte barrier function (asthma, allergic rhinitis)
  3. Drug-related eczematous - HR to drug
  4. Photoeczematous - abnormal reaction to UV/light
  5. Primary irritant forms - exposure to substances that damage skin
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9
Q
  1. Inflammatory skin diseases:

Acute Eczematous Dermatitis Pathogenesis

A

ALLERGIC CONTACT DERMATITIS
initial cutaneous exposure to environmental sensitizing agent ⇒ self-proteins altered processed by epidermal Langerhans cells ⇒ migrate to LN ⇒ presents AG to T-cell ⇒ CD4+ T-cell migrate to affected site ⇒ cytokine release ⇒ recruit inflammatory cells + epidermal damage

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10
Q
  1. Inflammatory skin diseases:

Acute Eczematous Dermatitis Clinical features

A
  • pruritic, edematous, oozing plaques contaning vesicles and bullae
  • persistent AG stimulation ⇒ lesions hyperkeratotic, acanthosis + chronic
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11
Q
  1. Inflammatory skin diseases:

Erythema Multiforme Pathogenesis

A
  • self-limiting disorder - HR to infection + drugs
    • infections: HSV, mycoplasma, fungal
    • drugs: sulfonamides, penicillin, salicylates, hydantoins, antimalarials
  • skin-homing cytotoxic T-cells, CD4+ helper T-cells, Langerhans cells ⇒ respond to crossreactive AG of basal cell layer of skin and mucosa ⇒ damage tissue
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12
Q
  1. Inflammatory skin disease:

Erythema Multiforme Morpholgy + Clinical features

A

MORPHOLOGY:
- macules, papules, vesicles + blisters
- targetoid rash - red macule with eroded center
CLINICAL FEATURES:
- less severe: infection
- severe: erythema multiforme major, Steven-Johnson syndrome, toxic epidermal necrolysis
⇒ sloughing of epidermis, loss of moisture and infectious barriers
⇒ SJS: oral mucosal + fever involvement
⇒ TEN: most severe

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13
Q
  1. Inflammatory skin diseases:

CHRONIC TYPES

A
  1. Psoriasis
  2. Lichen planus
  3. Lichen simplex chronicus
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14
Q
  1. Inflammatory skin diseases:

PSORIASIS pathogenesis

A
  • immunologic disease with genetic + environmental factors
  • sensitized T-cells enter skin ⇒ accumulate in epidermis ⇒ secrete cytokines + growth factors ⇒ keratinocyte hyper proliferation ⇒ lesions
  • Koebner phenomenon: lesion induces in susceptible people by local trauma
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15
Q
  1. Inflammatory skin diseases:

PSORIASIS morphology

A
  • acanthosis
  • elongation of rete ridges, parakeratosis
  • Auspitz sign: bleeding points ⇒ dilated vessels in dermal papillae, occurring when scale is removed
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16
Q
  1. Inflammatory skin diseases:

PSORIASIS clinical features + treatment

A 
CLINICAL FEATURES:
 - location: elbow, knees, scalp, lumbosacral area, intergluteal cleft, glans penis
 - lesion: well-demarcated, salmon colored plaque covered by silvery scale
 - nail changes
TREATMENT:
 - NSAIDs
 - immunosuppressive agents
 - TNF antagonists
 - UVA light with psoralen
17
Q
  1. Inflammatory skin diseases:

LICHEN PLANUS

A

PATHOGENESIS:
- expression of altered AG ⇒ CD8+ T cell mediated cytotoxic response
- associated with chronic hepatitis C virus
CLINICAL FEATURES:
- lesions: pruritic, purple, polygonal, planar papule, plaques
- self-limited (resolves in 1-2 years)
- Wickham striae
- location: wrist, elbow, oral mucosa
- saw-tooth appearance

18
Q
  1. Inflammatory skin diseases:

LICHEN SIMPLEX CHRONICUS

A
  • roughening of the skin
  • response, to local repetitive trauma
  • prurigo nodularis: localized to nodules
    PATHOGENESIS:
  • repetitive trauma ⇒ epithelial hyperplasia with dermal scarring
    CLINICAL FEATURES:
  • lesion: raised, erythematous, increased scale
  • often superimposed upon, masks another dermatosis
19
Q
  1. Inflammatory skin diseases:

ACUTE TYPES

A
  1. urticaria
  2. acute eczematous dermatitis
  3. erythema multiforme
  4. acne vulgaris
20
Q
  1. Melanocytic tumors:

COMMON MELANOCYTIC NEVI classification

A
  1. Junctional melanocytic nevus
    - dermal/epidermal junction
    - early development
  2. Compund melanocytic nevus
    - further development ⇒ dermis
  3. Intradermal melanocytic nevus
    - older lesions
    - pure dermal
21
Q
  1. Melanocytic tumors:

COMMON MELANOCYTIC NEVI pathogenesis

A
  • benign, well-circumscribed, round or ovoid lesions
  • derived from transformation of melanocytes
  • superficial nevus cells are larger + less mature - produce melanin, grow in nests
  • deeper nevus cells are smaller + mature - no pigment, grow in cords
  • neoplasm grow ⇒ migrate up or down
  • activating mutation in BRAF or RAS
22
Q
  1. Melanocytic tumors:

DYSPLASTIC MELANOCYTIC NEVI

A 
- atypical nevus
PATHOGENESIS:
 - sporadic: malignant transformation low
 - familial: AD, precursor to melanoma
MORPHOLGY:
 - compound nevus
 - fuse with other nests
 - lentiginous hyperplasia
 - cells show atypia
 - decreased level of melanin
23
Q
  1. Melanocytic tumors:

MALIGNANT MELANOMA types

A
  1. lentigo maligna melanoma
  2. superficial spreading
  3. nodular
  4. acral lentiginous
24
Q
  1. Melanocytic tumors:

MALIGNANT MELANOMA pathogenesis

A
  • sun exposure
  • preexisting nevi and hereditary predisposition
    • mutations in CDKN2A, BRAF, NRAS, PTEN
      Radial growth:
      ⇒melanoma grows horizontally within epidermis (no metastasis or angiogenesis)
      Vertical growth:
      ⇒ melanoma grows downward without cellular maturation
      ⇒ metastasis predicted by measuring depth of invasion
      Metastasis:
      ⇒ indicators: lymphatic density, mitotic rate, overlying ulceration
      ⇒ regional LN, liver, lung, brain etc
25
Q
  1. Melanocytic tumors:

MALIGNANT MELANOMA morphology + clinical features

A

MORPHOLOGY:

  • variation of pigmentation
  • irregular borders + often notched

CLINICAL FEATURES:

  • location: skin, oral + anogenital mucosa, esophagus, meninges, eye
  • usually asymptomatic, itching
26
Q
  1. Melanocytic tumors:

Staging of melanoma

A
  • Clark
  • Breslow
  • ABCDE
    • A - asymmetry
    • B - border
    • C - color
    • D - diameter
    • E - evolving
27
Q
  1. Non-melanocytic skin tumors:

TYPES

A 
BENIGN:
 - seborrheic keratosis
 - sebaceous adenoma
 - actinic keratosis
MALINGNANT:
 - squamous cell carcinoma
 - basal cell carcinoma
28
Q
  1. Non-melanocytic skin tumors:

SEBORRHEIC KERATOSIS

A
  • age: middle-aged and older
  • lesion: localized proliferation of basal cells - raised, round, coin-like warty lesion
  • arise spontaneously
  • location: trunk, extremities, head, neck
    PATHOGENESIS:
  • activating mutation FGF receptor 3
  • explosive onset ⇒ paraneoplastic syndrome
29
Q
  1. Non-melanocytic skin tumors:

SEBACEOUS ADENOMA

A
  • head and neck region in older people
  • flesh-colored papule + lobular proliferation of sebocytes
    PATHOGENESIS:
  • associated with Muir-Torre syndrome
  • internal malignancy, often colon carcinoma
    CLINICAL FEATURES:
  • benign, self-limited growth
30
Q
  1. Non-melanocytic skin tumors:

ACTINIC KERATOSIS

A 
- premalignant lesion with progressive dysplastic changes
MORPHOLOGY:
 S - solar elastosis
 P - parakeratosis
 A - atypia
 I - inflammation
 N - not-full thickness
PATHOGENESIS:
 - mutation of p53 (UV light injury)
CLINICAL FEATURES:
 - lesion: small, tan-brown, red colored + rough, sand-paper like consistency
 - predilection for sun-exposed area + accumulate with age
 - cryotherapy
31
Q
  1. Non-melanocytic skin tumors:

SQUAMOUS CELL CARCINOMA pathogenesis

A
  • risk factors: sun, industrial carcinogen, chronic ulcer, old burn scar, arsenicals, ionizing radiation

PATHOGENESIS:

  • UV light ⇒ p53 mutation (NOTCH, HRAS)
  • UV light ⇒ transient immunosuppressive effect ⇒ tumorigenesis
32
Q
  1. Non-melanocytic skin tumors:

SQUAMOUS CELL CARCINOMA morphology + clinical features

A

MORPHOLOGY:

  • sharply defined, red, scaling plaque
  • histo: high atypic, nuclear crowding, disorganization

CLINICAL FEATURES:

  • metastasis depend on: thickness + degree of invasion
  • tumors arising from actinic keratosis: less aggressive
  • mucosal squamous cell carcinoma more aggressive
33
Q
  1. Non-melanocytic skin tumors:

BASAL CELL CARCINOMA pathogenesis

A
  • slow growing, rarely metastasize
  • chronic sun exposure, light pigmented people
    PATHOGENESIS:
  • dysregulation of the sonic hedgehog PTCH ⇒ loss of heterozygosity in numerous individual tumor foci ⇒ Gorlin syndrome
  • p53 mutation
34
Q
  1. Non-melanocytic skin tumors:

BASAL CELL CARCINOMA morphology + clinical features

A

MORPHOLOGY:

  • pearly papule with prominent, dilated sub epidermal blood vessels
  • melanin pigments
  • histo: multifocal growth from epidermis, nodular lesions growing downward into dermis

CLINICAL FEATURES:

  • local excision as treatment
  • lesion can ulcerate
  • can lead to facial sinus or bone infiltrate

PATHOLOGY 2 (11 decks)

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