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  • Pathophysiology of Rheumatoid Arthritis

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    Gerardeanne Reposar
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    Rheumatoid arthritis is caused by a combination of genetic and environmental factors that lead to an autoimmune response. The immune system mistakenly attacks the joints, causing inflammation. This involves the activation of T cells, B cells, macrophages, and other immune cells that release cytokines and enzymes which damage cartilage and bone. Over time, this chronic inflammation can destroy joint structures and cause disability.

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    Pathophysiology

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    Rheumatoid arthritis is caused by a combination of genetic and environmental factors that lead to an autoimmune response. The immune system mistakenly attacks the joints, causing inflammation. This involves the activation of T cells, B cells, macrophages, and other immune cells that release cytokines and enzymes which damage cartilage and bone. Over time, this chronic inflammation can destroy joint structures and cause disability.

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    1K Ansichten1 Seite

    Pathophysiology of Rheumatoid Arthritis

    Hochgeladen von

    Gerardeanne Reposar
    Rheumatoid arthritis is caused by a combination of genetic and environmental factors that lead to an autoimmune response. The immune system mistakenly attacks the joints, causing inflammation. This involves the activation of T cells, B cells, macrophages, and other immune cells that release cytokines and enzymes which damage cartilage and bone. Over time, this chronic inflammation can destroy joint structures and cause disability.

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    © All Rights Reserved
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    von 1

    PATHOPHYSIOLOGY OF RHEUMATOID ARTHRITIS

    MODIFIABLE & NONMODIFIABLE FACTORS


    ENDOTHELIA
    ACTIVATION

    CD4 + T
    CELL
    CYTOKINES
    MACROPHAG
    E
    ACTIVATION

    B CELL
    ACTIVATION
    FORMATION OF
    RHEUMATOID
    FACTOR
    IMMUNE COMPLEX
    FORMATION AND
    DEPOSITION

    FIBROBLASTS
    CHONDROCYTES
    SYNOVIAL CELLS

    EXPRESSION OF
    ADHESION
    MOLECULES

    PROLIFERATI
    ON

    RELEASE OF
    COLLAGENASE,
    STROMELYSIN,
    ELASTASE, PGE2 AND

    JOINT

    PANUS FORMATION; DESTRUCTION OF BONE,


    CARTILLAGE; FIBROSIS; ANKYLOSIS

    ACCUMULATION OF
    INFLAMMATORY
    CELLS

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