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1.3: Why Me?, Physical examination, Full blood count, X-Rays of Hands +…

- - - - Joints affected are characteristic of RA
- - - - Psychological therapy
        
        Progressively developed pain and stiffness over 8 months, progressive loss of strength
        
        Unable to perform daily duties at home and family fruit farm
        
        Progressive loss of function
      - Stop smoking
        (highest impact environmental factor)
      - Pharmacological therapy
        
        DMARDs to induce disease remission, sslow disease progression, and improve long-term outcome
        
        Start with methotrexate (20mg weekly) and prednisolone (7.5mg daily) for 3 months - corticosteroid for control of inflammation until DMARD begins to take effect
        
        If ongoing active disease, add (combination therapy) or switch to 2nd DMARD for 3 months: sulfasalazine, leflunomide and/or hydroxychloroquine
        
        If still ongoing active disease, add (combination therapy) or switch to biological or targeted DMARD, most commonly TNF inhibitor
        
        Symptomatic treatments to improve patient QoL while waiting for DMARDs to take effect
        
        Analgesics (normal hierarchy of escalation)
        
        Anti-inflammatories
        
        NSAIDs and COXIBs
        
        Corticosteroids
- - - - Increased vascular flow
        
        Fluid extravasation leads to oedema
        
        Increased intra-joint pressure creates a hypoxic environment
        
        Type B synoviocytes respond by producing HIF1α, which is stabilised by IL-16 and TNF from Type A synoviocytes
        
        HIF1α causes production of VEGF, which stimulates poorly ordered angiogenesis, including formation of high endothelial venules
        
        Pannus formation (collection of reactive synovium, inflammatory cells, fibroblasts and granulation tissue)
        
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        Fibrinogen extravasation leads to formation of rice bodies
        
        Type A synoviocyte recruitment driven by TNF, IL-6, IL-1 from Type B synoviocytes
        
        Fusion into giant cells driven by IFNγ, IL-3 and GM-CSF
        
        Production of MMPs, decrease in TIMPs (MMP inhibitors)
      - Endothelial activation
        
        Recruitment of neutrophils in the synovial fluid by IL-8
        
        Joint aspirate
        
        Elevated WBC count
        
        20,000 x 10^6/L indicative of inflammatory condition
        
        Metabolism results in free oxygen radicals
        
        Activation of several enzymes
        
        Destruction of bone and cartilage (occurs at bare area within joint capsule where bone is covered with synovial membrane but not articular cartilage)
        
        Destruction of tendons, ligaments and joint space
        
        Joint subluxation and deformity
        
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      - Type B synoviocyte proliferation driven by TNF, IL-6, IL-1 from Type A synoviocytes (and autocrine bFGF)
        
        Hyperplasia of synovial membrane, resulting in 5-10 layers of synoviocytes (decreased apoptosis driven by epigenetic changes, including decrease in p53)
        
        Production of TNF, IL-17, TGFbeta, M-CSF and RANKL, stimulating osteoclasts
      - Accumulation of CD4+ T cells, particularly Th1 and Th17 cells
    - - Serology - Antibodies
        
        Elevated RF and anti-CCP
        
        Normal ANA
        
        Likely also excludes Sjogren's and scleroderma