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12 Cards in this Set
- Front
- Back
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What is pemphigus?
Mechanism? Intraepidermal bullae/superficial vesicles, skin/mucosa involved, Jewish/Mediterranean presdisposition: |
Autoimmune skin disease, blistering of skin/mucous membranes, Ab's against desmosomes, results in separation of epidermis
Type II Hypersensitivity (Ab + Ag, no lymphocytes) Pemphigus vulgaris |
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Pemphigus vulgaris:
Susceptibility due to what HLA? IGG's against what protein? What is bullous pemphigoid? IGG's against what proteins? |
D4, D6
desmoglein 3 chronic, autoimmune, subepidermal blistering skin, doesn't usually involve mucous membranes; IGG's bind to basement membranes hemidesmosomes - BP Ag 1, 2 (2 is more pathogenic) |
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What is eotaxin?
What IL may attract eosinophils to the skin? Newly exposed Ag's create new Ab's, polyclonal activation: Role of CD4+ T-cells? |
eos-specific chemokine, strongly expressed in BP lesions
IL-5 epitope spreading attract MMP's - destroy connective tissue |
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Autoimmune blistering disease, primarily affect mucous membranes, conjunctiva and skin:
Clinical presentation? Auto-Ab's against what? |
Mucous membrane pemphigoid
cutaneous involvement, tense blisters/erosions on head/neck, trauma sites epidermal-dermal junction |
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Autoimmune blistering disorder associated with gluten-sensitive enteropathy:
Diagnosis? Ab against what? |
Dermatitis herpetiformis
immunofluorescence of skin biopsy showing IGA deposition in papillary dermis epidermal transglutaminase 3 |
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Vitiligo:
Pathology and common co-diseases: Alopecia Areata: Pathology? What cytokines inhibit hair growth? |
progressive disorder, melanocytes are destroyed by CD8+ autoreactive cells; thyroid abnormalities common - Hashimoto's, Grave's disease
CD4+/CD8+ T-cell mediated destruction of hair; IL-1, TNF inhibit hair growth |
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Atopic dermatitis:
Pathology? What type of immune response? Often associated with what? |
T-cell mediated exaggerated cutaneous immune response to environmental Ag's
Th2 response - Ag specific IGE binds to mast cells causing degranulation, Type I hypersensitivity Associated with asthma, allergic rhinitis |
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Allergic contact dermatitis:
Pathology? Classic example? |
T-cell dependent, delayed Type-IV hypersensitivity reaction - Ag's form complexes with skin proteins, cause T-cell activation, cytokine release --> cell damage
Poison ivy |
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Characterized by red, scaly cutaneous plaques containing inflammatory infiltrates, epidermal hyperproliferation:
Mechanism? Mediated by what cells? Effect of UV treatment? |
psoriasis
Type IV hypersensitivity - Th1 response CD8+ T-cells reduces number of activated T-cells in epidermis/dermis |
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Cutaneous drug reactions:
Pathology? Anti-Ro auto-Ab's, reaction due to UV-modulation of auto-Ag's: |
Type III hypersensitivity, drugs attach to IGG, activates complement --> inflammation, fever, urticaria, kidney damage
Cutaneous lupus erythematosus |
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Characterized by neutrophilic transmural inflammation of vessel walls with fibrosis:
Often associated with what? |
Cutaneous vasculitis
new medications, infectious agents |
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What is cryoglobulinemia?
Differences between Type I, II, III? Involves IGG, often seen with SLE, RA: |
cryoglobulins precipitate at cold temperatures - Type III hypersensitivity activates complement
Type I - monoclonal IGG Type II - RF containing, monoclonal Type III - RF, polyclonal systemic sclerosis |
