allergic contact dermatitis uisu 110324
DESCRIPTION
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Allergic Contact Dermatitis
H M Nadjib Dahlan Lubis
Bag Patologi Anatomi Fak Kedokteran USU / UISU Medan
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Inflammatory Dermatoses
- Urticaria
- Acute Eczematous Dermatitis
- Erythema Multiforme
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Acute Excematous Dermatitis
- red, papulovesicular, oozing, & crusted, pruritic (itchy)
- Categories : - allergic contact d
- atopic d
- drug-related eczematous d
- photoeczematous d
- primary irritant d
- pruritic, edematous, oozing plaques, small/large blister
- bact yellow crust (impetiginization)
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Acute Excematous Dermatitis
- red, papulovesicular, oozing, & crusted, pruritic (itchy)
- Categories : - allergic contact d
- atopic d
- drug-related eczematous d
- photoeczematous d
- primary irritant d
- pruritic, edematous, oozing plaques, small/large blister
- bact yellow crust (impetiginization)
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Morphology
- spongiosis
- >< urticaria: superficial dermis, AED: intercell epid
- ingested drug lcy & eos: deep & superf dermal vessels
- contact Ag superficial
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I. Anaphylactic
II. Ab >< Ag: surface, tis componet
- Complement-Dependent Reactions
- Ab-Dependent Cell-med Cytotoxicity
- Ab-Mediated Cellular Dysfunction
III. Imm Complex Mediated
- Generalized
- Localized
IV. Cell Mediated
- Delayed-Type
- T-Cell Mediated Cytotoxicity
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Type I ( Anaphylactic )
Ag + Ab ( mast & baso ) * Mast (jar), baso (drh)
2 phases: - Initial : dil, leakage, spasm, 5-10 expos, 60 - Late : - 2-8 hari without expose several days - Eos, net, baso, mon - Destruksi mucosa epitel
Mast & baso : - Ig E Fc receptor - C 5a, C3a (anaphylatoxin) - IL8 (cytokine mac) - Codein, morphine - Mellitin (bee venom) - Phy : heat, cold, sunlight
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Type I hypersensitivity
- within minutes after Ag + Ab bound to mast cell allergy
- systemic injection
- local: - skin,
- nasal,
- conjunctiva,
- hay fever,
- bronchial asthma
- allergic gastroenteritis
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- immediate/ initial: - vasodilatation
- vasc leakage
- smooth muscle spasm
- glandular secretion
- 5-30’ after exposure, subside in 60’
- late phase reaction
- 2-24 h later, w.o. Additional exposure, last for
several days
- infiltration of eos, net, bas, mon, CD4 T cells
- tissue destruction: mocosa
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Central role of Th2
- in response to Ag & other: IL-4 T cells differentiate TH2
- TH2 IL-4 B cell class swithing to IgE
development of additional TH2
IL-5 development & activation of eosinophils
IL-13 IgE
mucous secretion
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Alergen APC (Dendritic) CD4 + T : TH2
cytokine
Ig E ( B cell)
Rec Fc Ig E (Mast, Bas)
Reexposure
Mediator
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Type II
Mediated by Ab >< Ag: surface of cells other tis. comp
- Complement-Dependent Reactions
- Antibody-Dependent Cell-Mediated Cytotoxicity
- Antibody-Mediated Cellular Dysfunction
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Complement-Dependent Reactions
- Transfusion reaction s - Erythroblastosis Fetalis - Autoimm hemolytic anemia, agranolocytosis, thrombocytopenia - Pemphigus Vulgaris - Certain Drug Reactions
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Antibody-Dependent Cell-Mediated Cytotoxicity
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Antibody-Mediated Cellular Dysfunction
- MyasteheniaGravis - Pemphigus Vulgaris, - Graves diseaase
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Type III
Ag-Ab comp activate complement sys damage
Ag: - exogen: foreign protein, bacteria, virus
- endogen: nucl Ag, Ig, Tumor Ag
Can be: - Generalized (Sys Imm Comp dis): Ag >>
- Localized (Arthus Reaction) : Ab >>
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Type IV: Cell Mediated Hypersensitivity
Initiated by Ag-activated (sensitized) T L’cyte
Includes: - Delayed-type: by CD4 T-cells
- Direct cell cytotoxicity: by CD8 T-cells
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T Cell-Mediated (Type IV) Hypersensitivity
- initiated by ag-activated (sensitized) T lcy, inc: CD4 & CD8
- CD4+ T cell-mediated hypersens - environmental Ag
- sel-Ag
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CD4 : - = Helper cell
- Cytokines B cell, NK, M’phage
- destroyed by HIV
Subsets: - TH1 IL-2, IFN Cell-mediated Immunity
- TH2 IL-4, IL-5 Humoral Immunity
Cytokines pathogenesis of Type I inc. Bron. Asthma
CD8 : - like CD4 secrete cytokine
- best: - virus
- tumor cells
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Delayed Type
Tuberculin Reaction: Reddening, Induration:
8-12 hrs, peak: 24-72 hrs subside.
Morp: - Mononuclear perivascular cuffing
- Permeability edema, fibrin
- L’cyte is replaced by M’phage: 2-3 wks
- M’phage Epitheloid Cells
- E’loid surrounded by L’cyte Granuloma
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Sequence
1. First Exposure CD4 recognize peptides bacilli +
class II mol on surface of M’cyte, Langerhans)
Sen CD4 TH1
2. Inj of Tuberculin memory TH1 + Ag (surface APC) activated, blast transformation, proliferation secrete cytokines IL-12
IFN-
IL-2
TNF-
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Common examples:
- Contact dermatitis
- Type I diabetes
- Multiple sclerosis
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T Cell-Mediated Cytotoxicity
Sensitized CD8+ T cells (CTL) kill Ag-bearing target cells
Role: - Graft Rejection
- Viral Infection
Viral Peptides + Class I complex on surface
Complex is recognized by TCR of CD8+ T L’cyte
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2 mechanisms of CTL killing
1. Perforin-granzyme-dependent killing2. Fas-Fas ligand-dependent killing
Perforin & Granzyme: Mediators in lysosome like granules in CTL
Perforin perforate plasma membrane
Granzyme: protease via pores Apoptosis
Activated CTL Fas-ligand ~ TNF-alpha + Fas (on target cells)
Apoptosis
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Reaction of CD4: Delayed-Type Hypersen & Immune Inflammation
- DTH to: - exogen Ag
- self-tissue
- ass. w. - TH1 : activated macrophages
- TH17: neutrophil
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Causes
Inside : reaction to an internal circulating antigen food or drug).Outside : application of antigen (such as poison ivy) poison ivy/oak (Rhus toxicodendron),
characterized by pruritic, edematous, oozing plaques, often containing small and large blisters (vesicles and bullae) ( Fig. 25-24A ). prone to bacterial superinfection yellow crust (impetiginization). less “wet” (fail to ooze or form vesicles) , (hyperkeratotic) (acanthosis).
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