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RHEUMATOID ARTHRITIS
Saurabh Garg
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Rheumatoid Arthritis
Chronic multisystemic inflammatory disease of
unknown etiology
Affects the Synovial Membranes of multiple joints
Female : Male ratio 3:1
Most frequent during 4th and 5th decade
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PATHOGENESIS
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Normal Synovial Joint
Articular cartilage
Synovium Membrane
Lamellar bone
Subchondral bone
Type A cell: mphage like,
protective role
Type B cell:
fibroblast
like, produce
matrix and
synovial fluidVessel
Synovial Membrane:only 1-2 cells thick
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Thickened Synovium
Lymphocytic Infiltrate
Neovascularization
EARLY CHANGES IN RA
Major type of cells in synovium are T-cells and macrophages whereas in synovial fluid
neutrophils are neutrophils
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Destruction of Joint Cartilage and Bone
Proliferating synovial lining => Pannus
Proliferating synovial lining comes in
contact with the cartilage matrix and bone
there is degradation of the cartilage and
erosion of the bone surface (by matrix
metalloproteinases and other proteases
produced by synovial cells)
Chondrocytes themselves
IL-1 and TNF-alpha also stimulate production of
metalloproteinase by Chondrocytes of the
articular cartilage. In response to these
cytokines, chondrocytes decrease type IIcollagen and proteoglycan synthesis and
increase synthesis of metalloproteinases that
contribute to the degradation of collagen and
proteoglycans.
Neutrophils in Synovial Fluid
The main inflammatory cells of the
synovial fluid are neutrophils.
Cytokines such as transforming growth
factor beta (TGF-beta) and interleukin 8(IL-8) attract neutrophils.
Neutrophils may undergo degranulation
and cause some damage to surrounding
tissues.
Osteoclasts
Osteoclasts may be activated by
inflammatory mediators
including IL-1, TNF and PGE2
bone
cartilage
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Rheumatoid Arthritis
Clinical presentation
usually presents insidiously;
prodromal syndrome of malaise, weight loss and vague
periarticular pain and stiffness may be seen less commonly, the onset is acute, triggered by a stressful
situation such as infection, trauma, emotional strain or in
the postpartum period.
the joint involvement is characteristically symmetric withassociated stiffness, warmth tenderness and pain
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Rheumatoid Arthritis
Clinical Features
the stiffness is characteristically worse in the morning and
improves during the day; its duration is a useful indicator
of the activity of the disease.
the usual joints affected by rheumatoid arthritis are the
metacarpophalangeal joints, the PIP joints, the wrists,
knees, ankles and toes.
Entrapment syndromes may occur especially carpal tunnel
syndrome
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Rheumatoid Arthritis
After months to years, deformities can occur; the
most common are
ulnar deviation of the fingers
swan neck deformity, which is hyperextension of the distalinterphalangeal joint and flexion of the proximal
interphalangeal joint
boutonniere deformity, which is flexion of the distal
interphalangeal joint and extension of the proximalinterphalangeal joint
valgus deformity of the knee
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Extra-articular manifestations
Rheumatoid nodules
Vasculitis
Ocular manifestations
Keratoconjunctivitis sicca, episcleritis, scleritis, glaucoma
Pulmonary manifestations Pleural involvement, Fibrosing alveolitis , Obliterative
bronchiolitis Feltys Syndrome
- RA with Splenomegaly and neutropenia
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Extra-articular manifestations
Cardiac involvement Constrictive pericarditis
Renal involvement Secondary amyloidosis
Neurologic manifestations Mononeuritis multiplex, entrapment neuropathies, peripheral
neuropathies
Hematological Anemia
Thrombocytosis
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