Systemic chronic inflammatory disease characterised by nonsuppurative proliferative synovitis, destruction of articular cartilage and underlying bone with resulting disabling arthritis
extra-articular involvement -for example, of the skin, heart, blood vessels, muscles, and lungs-RA may resemble SLE or scleroderma
five times more common in women than in men
Joint pathology in RA:
symmetric arthritis, principally affecting the small joints of the hands and feet, ankles, knees, wrists, elbows, and shoulders
Morning or inactivity stiffness shows inflammatory nature of the joint disease
proximal interphalangeal and metacarpophalangeal joints are affected, but distal interphalangeal joints are spared.
Axial involvement, when it occurs, is limited to the upper cervical spine
radiographic hallmarks are joint effusions and juxta-articular osteopenia with erosions and narrowing of the joint space and loss of articular cartilage
Destruction of tendons, ligaments, and joint capsules
radial deviation of the wrist,
ulnar deviation of the fingers,
flexion-hyperextension abnormalities of the fingers
swan-neck deformity
boutonnière deformity
radiographic hallmarks
joint effusions
juxta-articular osteopenia
erosions and narrowing of the joint space
Microscopic features:
chronic synovitis with synovial cell hyperplasia and proliferation
dense perivascular inflammatory cell infiltrates (frequently forming lymphoid follicles) in the synovium composed of CD4+ T cells, plasma cells, and macrophages
increased vascularity due to angiogenesis
neutrophils and aggregates of organizing fibrin on the synovial surface and in the joint space
increased osteoclast activity in the underlying bone, leading to synovial penetration and bone erosion.
pannus, formed by proliferating synovial-lining cells admixed with inflammatory cells, granulation tissue, and fibrous connective tissue, which will cause enzymatic erosion of articular cartilage and subarticular bone
periarticular soft tissue edema
fibrosis and calcification may cause permanent ankylosis
Systemic features of RA:
Fever, wt loss and malaise due to IL1 and TNF alpha
Rheumatoid subcutaneous nodules
along the extensor surface of the forearm or other areas subjected to mechanical pressure
they can form in the lungs, spleen, heart, aorta, etc
central focus of fibrinoid necrosis surrounded by a palisade of macrophages, which in turn is rimmed by granulation tissue
fibrinous pleuritis or pericarditis
Lung: progressive interstitial fibrosis
Ocular changes such as uveitis and keratoconjunctivitis
Vasculitis and peripheral neuropathy
rheumatoid factor
are at risk of developing vasculitic syndromes;
autoantibodies that bind to the Fc portions of their own (self) IgG.
20% of patients do not have RF
Raynaud phenomenon
reactive amyloidosis
chronic, remitting-relapsing course
Treatment: DMARD and anti-TNF alpha
Pathogenesis of RA:
Exact cause in unknown
Association with HLA-DR4
increased frequency of this disease among first-degree relatives and a high concordance rate in monozygotic twins shows that the disease has some genetic component.
Infections withEBV, Borrelia species, Mycoplasma species, parvoviruses, and mycobacteria might be a triggering factor
Activation of B cells, macrophages, endothelium, fibroblasts, chondrocytes and synovial cells to form pannus,which causes enzymatic digestion of the cartilage and the underlying bone
autoantibodies that bind to the Fc portions of their own (self) IgG rheumatoid factor (RF) are formed
20% of patients do not have RF.
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