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