Arthritis

It’s Non-organ specific

Caused by wear and tear of joints causing inflammation Non-inflammatory disorder (use of synovial joints) Characterised by cartilage loss Affects knees, hips + small hand joints Link to obesity

Worsened by movement Eased by rest Worse at the end of the day Commonly affects: • hands • knees • spine • hips Unilateral (affect only one joint e.g. left hand only)

Steroid injections NSAIDs / Cox-2 inhibitors Surgery - knee replacement

NSAIDs inhibit COX enzyme

In Arthritis, NSAIDs block cyclooxygenase enzymes (particularly COX-2) which reduces inflammation, pain + stiffness COX enzymes convert arachidonic acid to prostaglandins

Intra-articular (into joints) When pain is moderate to severe Drugs: • triamcinolone • methylprednisolone Can cause cartilage injury + loss

Autoimmune disease in which the body’s immune system attacks the joints causing chronic inflammation.

Joint damage Muscle wastage Deformity

Pain Stiffness Joint swelling Joint deformity

WBCs = INCREASED Erythrocyte sedimentation rate (speed at which your red blood cells clump and fall together to the bottom of a glass tube within an hour) = INCREASED Anaemia Rheumatoid factor (group of proteins your body creates when your immune system attacks healthy tissue - Antibodies to IgG) = INCREASED

Age Gender - women developing premenopausal Post-partum Stress Genetics - if one twin has, the other is 20% likely Smoking

Improves movement Worse on waking Affects small joints Affects bilateral joints

Systemic disease (affects many organs or body as a whole) that affects: • Especially at the joints • Eyes inflammed (50%) • Skin • Vasculitis - destroy group of blood vessels • Lungs • Salivary glands (reduced) • Pericarditis (inflammation of pericardium)

Symptomatic relief • Analgesia to reduce need for NSAIDs • NSAIDs (+ PPI) Slow progression • DMARDs • Steroids • Biologicals Monitor effectiveness

Directly inhibits cell proliferation (inhibit wide variety of cytokines including interleukins, interferons + TNFalpha) Slow-acting (may take months for benefits to become apparent) No analgesic activity Used for rheumatic disorders + where inflammation does not respond to COX enzyme inhibitors Slows course of disease

1st LINE - Start w/ combination therapy (MTX + 1 other DMARD) 2nd LINE - Mono therapy w/ rapid dose titration Slow onset of action - take up to 3 months Used with glucocorticoids until effective (shouldn’t be used long term)

Dose increased gradually Improvement takes a few months Monitoring is necessary Nausea Signs of: • Blood dyscrasias (formed elements in blood) = sore throat, tiredness • liver toxicity = jaundice • lung toxicity Bone toxicity Perform LFTS, FBC + U+E before + during treatment

Methotrexate = 1st choice Sulfasalazine Leflunomide IM gold

Dihydrofolate reductase inhibitor (pyrimidine synthesis = inhibits DNA/RNA synthesis) Immunosuppressant Commonly used Dose - 7.5-25 micrograms Weekly dosing

Autoimmune diseases is when your immune system attacks its own cells Leads to tissue damage Genetic factors can influence it Can be influenced by pregnancy, infection, diet + environment

Within 3 months

Reduce to a dose when symptom control has been achieved

Folic acid To prevent side effects Folic acid does not prevent inflammatory effects of methotrexate