hyper sensitivity

Hypersensitivity : 

Hypersensitivity

Hypersensitivity (too much of a good thing) : 

Hypersensitivity (too much of a good thing) Immune .sys.reacts in an exaggerated / inappropriate way to a foreign substance. Allergy is another name of H.S Hypersensitivity refers to undesirable (damaging, discomfort producing and sometimes fatal) reactions produced by the normal immune system. Hypersensitivity reactions require a pre-sensitized (immune) state of the host

Type I Hypersensitivity : 

Type I Hypersensitivity It is also known as immediate or anaphylactic Hypersensitivity .

Type-I : : 

Type-I : Anaphylaxis is harmful result of IgE Ab’s It may be local (atopy) / genaralised Atopy:occur at site of entry-Wheal and flare reaction Allergen : is an ordinary harmless foreign sub.e.g:pollen,dander,mites,fleas&their faecalpellets&insect stings

Mechanism:(sensitization phase) : 

Mechanism:(sensitization phase) Initial exposure of B-cell activated memory B-cell plasma cell IgEprod’n attached to mast cell in R.T&basophils of blood

Activation phase: : 

Activation phase: 2 nd exposure of allergen IgE+allergen degranulation histamins&lukotriens mucus secretion&C.P dilatation anaphylaxis

Meadiators of H.s : 

Meadiators of H.s Pre formed: Histamines ; Chemotactic factors; Newly synthesized mediators Leucotriens; Thrombixins& PG(D2): Platelet activation factor; Treatment: Hyposensitization

Type II Hypersensitivity : 

Type II Hypersensitivity It is also known as cytotoxic hypersensitivity and may affect a variety of organs and tissues

Slide 11: 

It is antbody mediated Stimulated by binding of Ab to an Ag on the surface of a cell 3 mechanisms are involved: i)Complement mediated; ii)ADCC: iii)Ab mediated cellular disfuncton: e.g:myastheniagravis,transfusion reactions, Rh-incompatability reactions. Auto immune reactions: Idiopathic thrombocytopenia purpura

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Arthus reaction: in 1903 Thisis due to aggrevation of Ab&Ag Activation of complement & PMNL’s are imp. It may be ------i)systemic ii)localised Normally phagocytes & RBC having C3b receptors will remove with help of kuffer cells

Systemic immune complex diseases : 

Systemic immune complex diseases E,g serum sickness------by vanpirquit 3 phases i)complex formation ii)deposition iii)inflammatory reaction Size is imp here. Deposition sites:kidney, joints , heart& small vessels .

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Immune complex deposition in blood vessels

Localized immune complex diseases; : 

Localized immune complex diseases; Arthus reactions ____vasculitis In or near vessel wall(venuls) Result in rupture of vessels Necrosis of local tissue

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E.g : good pasture syndrome ,serum sickness, rheumatic fever Occupatiomal diseases;farmars lungs , bagassosis.

Type –IV : 

Type –IV Cell mediated / delayed type of H.S Initiated by Ag-specific T-cell’s cytokines release cascade reactions e.g tubarculin reaction

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Stages i)sensitization----1-2 week’s ii)challenge stage Ag specificT-cell+MHC-peptide APC’s t-cell activation(Th1) and Cytokines like chemokines, IF-?.IL-2 release macrophase activation ingestion degranulation by lysosomes&by products of Resp.burst if persistent Ag; granulomas caseous necrosis

Variants of DTH: : 

Variants of DTH: Contact sensitivity: eg poison ivy dermatitis pentadecacatecol lipid soluble haptons heptan carrier conugate APC(langerhan’s cells) Rx is patch test 2.Allograft rejactions; allogenic donar

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THANK YOU Submitted by: B.Rajendar Submitted to: Dr.Ananad kumar