Rhumatoid Arthtritis

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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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    THANK YOU