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Rheumatoid Arthritis: Pathophysiology and Treatment
Pathophysiology of Rheumatoid Arthritis
- Autoimmune Response: Activation of T-helper cells and release of cytokines like TNF-α, IL-1, and IL-6.
- Synovial Inflammation: Inflammatory cell infiltration causes pannus formation, eroding cartilage and bone.
- Joint Damage: Release of enzymes like MMPs leads to cartilage destruction and bone resorption.
Classification of Drugs Used in RA
- NSAIDs: E.g., ibuprofen, diclofenac.
- Corticosteroids: E.g., prednisone, methylprednisolone.
- DMARDs:
- Conventional Synthetic: Methotrexate, sulfasalazine, hydroxychloroquine.
- Biologic: TNF inhibitors (infliximab), IL-6 inhibitors (tocilizumab), B-cell depleters (rituximab).
- Targeted Synthetic: JAK inhibitors (tofacitinib).
Mechanism of Action and Adverse Effects
NSAIDs
- Mechanism of Action: Inhibit COX enzymes, reducing prostaglandin synthesis.
- Adverse Effects: Gastric ulcers, renal impairment, cardiovascular risks.
Corticosteroids
- Mechanism of Action: Suppress cytokine production and immune activation.
- Adverse Effects: Osteoporosis, hyperglycemia, infections.
Conventional DMARDs
- Methotrexate: Inhibits DNA synthesis. Adverse Effects: Hepatotoxicity, bone marrow suppression.
- Hydroxychloroquine: Inhibits antigen presentation. Adverse Effects: Retinopathy, myopathy.
Biologic DMARDs
- TNF Inhibitors: Neutralize TNF-α. Adverse Effects: Infections, malignancies.
- IL-6 Inhibitors: Block IL-6 receptor. Adverse Effects: Infections, liver enzyme elevations.
Targeted Synthetic DMARDs
- JAK Inhibitors: Block cytokine signaling. Adverse Effects: Infections, thrombosis.
