Inflammation : Hypersensitivity

An excessive and potentially harmful immune reaction to a foreign substance not otherwise considered to be noxious

Anaphylactic reactions mediated by IgE

Fungal spores House dust mites Pollen

Substance ingested into the body which is recognised as foreign to the body’s immune system resulting in an allergic reaction

Maintaining immunosuppression: Corticosteroids Treatment: Control flares or attacks with corticosteroids

Antibody-dependent cytotoxic hypersensitivity Antibody mediated destruction of cells

The antibodies produced by the immune response bind to antigens on the patient’s own cell surface.

IgM or IgG antibodies form competes with soluble antigen complexes become deposited in tissues where they activate inflammation, causing tissue damage Occurs in blood vessels, kidney, joints

Pathological reactions to environmental chemicals or persistent microbes (e.g. tuberculosis)

Dendritic cells present allergen to T-cells and B-cells This triggers an inflammatory response Allergens trigger a TH2 reaction IgE antibody is produced Mast cells present IgE, when allergen comes the mast cells releases (degranulates) its mediators (amines etc.)

Hypersensitivity = Eosinophils (Eos is sensitive to steroids = benefit) Inflammation = Neutrophil

Adrenaline injection - vasoconstriction Beta-adreno receptor agonist

IgM or IgG to cellular antigen -e.g. red blood cell from transfusion Antibodies opsonise cells, activate complete and own cells are phagocytksed.

IgM or IgG antibodies form complexes with soluble antigen These complexes become deposited in tissues where they activate inflammation then causing tissue damage. This occurs in blood vessels, kidneys and joints

Pathological reactions to environmental chemicals or persistent microbes (e.g. tuberculosis) Activates T-cells and cytokines