Pathophysiology of Rheumatoid Arthritis and Septic Arthritis

Submitted to: Mr. Dennis Glen Ramos

Submitted by: Chelsea Mae Nobleza

Risk Factors Genetic (HLA-DR4 on the short arm of chromosome 6) More common in women Age 35-50 y/o Viral Infections Smoking

Production of Rheumatoid factor against IgG

Deposition of immune complexes

Prostaglandin Release

IL-1 mediates inflammatory response

Macrophages are stimulated Stimulation of B and T cell proliferation in the subintimal area

Neutrophil in its inactive state accumulates in synovial fluid

Synoviocytes exposure to IL-1 Produces IL-6, PGE2 and MMPs which causes proteoglycan degradation

New blood vessel growth (angiogenesis) Early pannus invation and chondrocyte activation

Increase in severity of signs and symptoms

secrete proteolytic enzymes contributing to the dissolution of their own cartilage matrix. Progressive narrowing of joint spaces

IL-6 suppresses albumin synthesis by the liver and stimulates acute phase protein synthesis thus, Swelling in small joints contributes assoc. With pain, significantly to stiffness and fatigue high ESR elevation. Warm swollen effusions, pain and decreased motion with possible rheumatoid nodules Erosion of contiguous bone and cartilage and laxity of ligaments

oxygen-derived free radicals that depolymerize hyaluronic acid and inactivate endogenous inhibitors of proteases are released

Proteoglycan degradation is further compounded by IL1 and TNF by inducing synthesis of proteases and preventing its repair.

RHEUMATOID ARTHRITIS

SEPTIC ARTHRITIS RISK FACTORS Use of prosthetic joint N. gonorrhoea infection S. Aureus Osteomyelitis Use of Immunosuppressive agents Diabetic patients Lyme disease

Pathogenic Invasion and Proliferation

Reactive

Local Infection

S. aureus promotes tropism in the synovium by binding to specific tissue adhesion factors

N. gonorrhoea induces a mild influx of WBC into the joint

HLA-B27 exhibit molecular mimicry by presenting arthritogenic bacterial material to T-cells

Delayed healing related to PJIs

Absence of usual tissue barriers

S. aureus activates chondrocyte proteases

oxygen-derived free radicals that depolymerize hyaluronic acid are released Hosts polymorphnuclear leukocyte response is activated

Autoimmune response

Implanted hardware becomes less susceptible to infections by haematogenous spread as the pseudocapsule develops around it

Triggers bacteria altering selftolerance to B27 antigen

Altered host response in regard to enhanced invasion of microbes in the GUT facilitating persistent state of Chlamydia

Hydrolysis of essential collagen and proteoglycans Synovial hyperaemia with exudation of fluid Fluid has high fibrin content Rapid consumption of nutrients due to bacterial proliferation

Biofilm coagulase negative S. Aureus protects the pathogen from host defenses

Polymethylmethacrylate cement inhibits WBC

Cartilage nutrition is inhibited leading to destruction of cartilage cells

Pannus formation begins as well as large effusions

Cartilage erosion occurs at the lateral margins of the joints

Impairment of blood supply and may cause aseptic necrosis of the bone

References: Medical Surgical Nursing: clinical Management for Positive Outcomes by Black and Hawks Brunner and Suddarths Textbook of Medical Surgical Nursing www.emedicine.medscape.com/article/23699-overview#ao156 www.hoopkins-arthritis.org/arthritis-info/rheumatoid-arthritis/rheum_clin_path.html Rheumatoid arthritis by William et. al