Uploaded byJegan Nadar
Pathophysiology of Rheumatoid arthritis
Rheumatoid arthritis (RA) is a chronic autoimmune disease that causes joint inflammation, leading to pain, stiffness, and potential joint damage and deformity. It primarily affects women and often begins in middle age, with symptoms including joint pain, swelling, and deformity. Diagnosis is made through physical exams and tests, with treatment options like NSAIDs, steroids, and surgery available.
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Rheumatoid arthritis (RA) is a chronic autoimmune disease affecting joints, causing pain, stiffness, and joint damage, primarily in women.
RA involves the immune system attacking the synovial membrane, activating T-cells, and leading to the production of damaging cytokines and enzymes.
Key symptoms include joint pain, swelling, and stiffness. Diagnosis involves physical exams and various tests such as blood tests and imaging.
Treatment options include NSAIDs, steroids, DMARDs, and surgical procedures like synovectomy and total joint replacement.
Closing presentation.
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Pathophysiology of Rheumatoid arthritis
- 1. PREPARED BY: JEGAN.S. NADAR RHEUMATOID ARTHRITIS
- 2. RHEUMATOID ARTHRITIS Rheumatoidarthritis (RA) is a chronic autoimmune disease. It causes joints to swell and can result in pain, stiffness, and progressive loss of function. RA often affects pairs of joints (both hands, both feet, etc) and can affect more than one joint, including the small joints in the wrists and hands. Over time, other joints can be affected such as shoulders, elbows, knees, feet, and ankles. Jegan
- 3. Over time,the inflammation of RA can cause damage to the joints. In some patients, this may lead to permanent joint damage. As this joint damage progresses, in severe cases, it can cause deformity of the joints and loss of function. It may begin to interfere with daily activities, making them more difficult and painful to do RA often begins in middle age, but can start at any age. RA affects 2 to 3 times as many women than men. Jegan
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- 5. PATHOPHYSIOLOGY Rheumatoid arthritisis autoimmune disorder in which Immune system identifies the synovial membrane as "foreign“ and begins attacking it With long-term or intensive exposure to the antigen, normal antibodies become auto-antibodies that target self-antigens in the synovial membrane. Once the antigen or immune complex reaches the synovial membrane .The antigen presenting cell deals with it. Jegan
- 6. First, theAntigen Presenting Cell usually a macrophage in synovium engulfs the antigen. Enzymes (peroxides) inside the APC break down the antigen into smaller particles The processed antigens are transported to the surface of the APC Antigen is now presented to T-cells (CD4 cells ie. T-helper cell ) or CD8 (cytotoxic T cells) which the T-cell receptor (TCR) recognizes and binds to. Jegan
- 7. Once theT-cell binds to the Antigen it becomes activated, the APC then secrete cytokines like Interleukin-1 (IL-1) Interferon-alpha (IFN-a) Interferon-gamma (IFN-g) Tumor necrosis factor (TNF) APC also Secretes Lysozymes, Elastases and Collagenases these enzymes cause cartilage breakdown. Jegan
- 8. On exposureto IL-1, synoviocytes proliferate and produce following factors Interleukin-6 (IL-6) Prostaglandin's (e.g. , PGE2) , and platelet-activating factor, which are involved in the pain mechanism. Matrix Metalloproteases that cause activation of collagenase, an enzyme required for cartilage breakdown. Jegan
- 9. SYMPTOMS Joint pain Joint tenderness Joint swelling Joint redness Joint warmth Joint stiffness Many joints affected (polyarthritis) Joint deformity Both sides of the body affected (symmetric) Jegan
- 10. DIAGNOSIS Physical examination Blood test Antibody test ESR X-Ray MRI Jegan
- 11. TREATMENT NSAIDs Steroids. Disease-modifying antirheumatic drugs (DMARDs) Surgery Synovectomy Tendon repair Total joint replacement Jegan
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