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Modifiable - Environmental Factors a. Medications (antidepressants/ antibiotics) b. Extreme stress c. Exposure to sunlight/UV radiation d. Infections e. Hormonal changes Non Modifiable - Genetics - Gender - Age - Race

Production of abnormal antibodies by B cells (hallmark sign), (antidouble stranded DNA & anti smith) Few tingible body macrophage ( engulf B cells that have undergone apoptosis after somatic hypomutation) Dec./ missing/ deficient CRP & glycoproteins (complement factors for efficiently operating phagocytes)

Abnormal reaction of body against its own cells and serum protein

Increased level of anti ds DNA antiobodies Results to engulfed LE bodies in the LE cells Increased disease activity in client w/ SLE ANA and nuclear antigen found in serum, small blood vessels, skin & glomelular basement membrane immune complexes initiate the complement reaction & serum complement level are decreased during attacks of SLE

Degeneration of connective tissues, glomeruli, blood vessels

Increases in self & non self antigen Hyperactivity of B cells Immune complex deposition, Antineurral, antibody activity

Specific antigen in joints (T lymphocytes) Release lymphokines RH factor (IgM, IgG) on antigen in synovial Cavity stimulated by self antigen (an antigen in the synovial cavity or an infectious antigen) RF IgG complexes are present in rheumatoid lesions and apparently activate complement to promote the inflammatory response acute attacks of rheumatoid arthritis occur as the RF-IgG complexes precipitate in synovial fluid Complement is activated that attacks polymorphonuclear leukocytes, whose main function appears to be phagocytes of the complexes liposomal enzymes released by this cells intensify inflammation

granulation tissue and inflammatory cells form a mass of tissue called PANNUS that erodes the articular cartilage the joint space is destroyed, and the resultant scarring may completely immobilize the joints or cause bleeding and thrombus in the area swelling & pain, warm skin, during RA attacks