Rheumatoid Arthritis Pathophysiology (signs and symptoms)
Armando Hasudungan
15 min, 34 sec
A comprehensive overview of rheumatoid arthritis including its symptoms, joint effects, cellular level pathophysiology, potential causes, and extra-articular manifestations.
Summary
- Rheumatoid arthritis (RA) is a systemic rheumatological disorder that causes symmetrical arthritis with early hand involvement, affecting metacarpal phalangeal and proximal interphalangeal joints.
- RA leads to characteristic hand deformities such as swan neck, boutonniere deformity, and 'Z' deformity of the thumb, along with ulnar deviation.
- At the cellular level, RA involves inflammation of the synovial membrane, angiogenesis, and the activation of immune cells leading to bone and cartilage degradation.
- Potential causes of RA include genetics, environmental factors, and autoantigen modifications like citrullination, which the immune system mistakenly targets.
- Extra-articular manifestations of RA can affect skin, liver, heart, muscles, bones, and lungs, often exacerbated by treatments like glucocorticoids.
Chapter 1
An introduction to the clinical presentation of rheumatoid arthritis.
- Rheumatoid arthritis is introduced as a systemic disorder affecting multiple joints.
- Symptoms include symmetrical arthritis with pain, swelling, and nodules, particularly in the hands.
- Contrasts with osteoarthritis, which affects different joints.
Chapter 2
A detailed look at how rheumatoid arthritis affects the joints, especially in the hands.
- RA commonly affects metacarpal phalangeal and proximal interphalangeal joints early in the disease.
- Typical deformities discussed include swan neck, boutonniere deformity of the thumb, and ulnar deviation.
- These deformities are explained in detail, illustrating the changes in joints and fingers.
Chapter 3
Exploring the cellular-level changes in the joints due to rheumatoid arthritis.
- The structure of a typical joint and the role of the synovial membrane, synovial fluid, and cartilage are recapped.
- The process of synovitis in RA is described, leading to bone and cartilage erosion.
- Cells involved in RA include macrophages, fibroblast-like synoviocytes, T cells, plasma cells, and neutrophils.
Chapter 4
Understanding how inflammation and immune cell migration contribute to the symptoms of rheumatoid arthritis.
- Cytokines from immune cells cause inflammation and joint damage.
- Activated fibroblast-like synoviocytes can migrate between joints, explaining symmetrical joint involvement.
- The role of T cells and B cells in promoting inflammation and bone erosion is discussed.
Chapter 5
Examining potential causes and triggers that might lead to the onset of rheumatoid arthritis.
- While the exact cause of RA is unknown, several theories exist, including genetic and environmental factors.
- Autoantigen modifications, such as citrullination, may lead the immune system to attack the body's own tissues.
- The process of immune system activation, including antigen-presenting cells, T cell activation, and antibody production, is outlined.
Chapter 6
Discussion on the key antibodies involved in rheumatoid arthritis and their implications.
- Rheumatoid factor (IgM) targets the IgG antibodies and forms immune complexes, present in 75% of RA cases.
- Anti-citrullinated protein antibodies (ACPA) are specific to RA and target proteins that have undergone citrullination.
- Both types of antibodies are significant in diagnosing RA and contribute to its pathophysiology.
Chapter 7
Exploring how rheumatoid arthritis affects other organs and systems beyond the joints.
- Extra-articular manifestations result from cytokines produced by immune cells in the joints.
- Effects include skin nodules, liver inflammation, cardiovascular issues, neurological symptoms, musculoskeletal complications, and lung problems.
- These conditions can be worsened by RA treatments, such as glucocorticoids, which suppress the immune system.
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