Treatment Goal of treatment reduce inflammation and pain preservation of function prevention of deformity.

Non-pharmacological therapy Education Aerobic conditioning Reduction of adverse mechanical factors Exercise Strengthening Pacing of activities Weight reduction if obese

pharmacological therapy *simple analgesic drugs *NSAIDs *Topical creams * Opioid analgesics *Amitriptyline 'disease-modifying antirheumatic drug' ((DMARD *Corticosteroids Local injections Surgery

in RA comprises the early Treatment in RA comprises the early use of disease-modifying antirheumatic drugs (DMARDs), and corticosteroids for induction of remission. There is evidence that early use of DMARD therapy improves clinical outcome in RA. Partial or nonresponse to DMARD therapy should prompt progression to biological drugs if necessary

1-SIMPLE ANALGESIA Paracetamol (1 g 6-8-hourly) is the oral analgesic of choice because of its efficacy, lack of contraindications or drug interactions, long-term safety, low cost and availability. Paracetamol inhibits prostaglandin synthesis centrally in the brain but has little effect on peripheral production of prostaglandins

2-NON-STEROIDAL ANTI-INFLAMMATORY DRUGS (NSAIDS) These are among the top five most prescribed drugs in many countries. Oral NSAIDs are often effective for the pain and stiffness of inflammatory disease. Long-acting NSAIDs given at night are particularly helpful for marked inflammatory early morning stiffness. NSAIDs may also reduce bone pain due to secondary malignant lesions.

The major drawback of NSAIDs is gastrointestinal toxicity The major drawback of NSAIDs is gastrointestinal toxicity. Prostaglandins of the E series play a major role in gastroduodenal defence mechanisms. By depleting mucosal prostaglandin levels, aspirin and NSAIDs impair this 'cytoprotection', resulting in mucosal injury, erosions and ulceration. NSAIDs are an important aetiological factor in up to 30% of gastric ulcers.

RISK FACTORS FOR NSAID-INDUCED ULCERS *Age > 60 years *Past history of peptic ulcer *Past history of adverse event with NSAIDs *Concomitant corticosteroid use *High-dose or multiple NSAIDs *Individual NSAID-highest with piroxicam, ketoprofen; lower with ibuprofen

3-CORTICOSTEROIDS IN RHEUMATOID ARTHRITIS Systemic corticosteroids have disease-modifying activity, but their primary role is in the induction of remission in patients with early RA who are starting synthetic DMARD treatment. Various regimens have been used One strategy is to give a high dose of oral prednisolone initially (60 mg daily) and to reduce and stop this gradually over a period of 3 months as the DMARD starts to take effect.

Intra-articular corticosteroids are primarily indicated when there are one or two ‘problem joints’ with persistent synovitis despite good general control of the disease. Although corticosteroids are very useful, they also have significant adverse effects., osteoporosis is probably the most important since this is a known complication of RA, even in the absence of corticosteroid therapy. Accordingly DEXA scanning followed by bone protection should be considered in any patient with RA who is expected to be on more than 7.5 mg prednisolone daily for more than 3 months

4-‘Disease-modifying antirheumatic drugs DMARDs

Classification of DMARDs 1-Non-Immunosuppressive agents 2-immunosuppressive agents 3-Biological agents 15

a-Non-Immunosuppressive agents Sulfasalazine Hydroxychloroquine Gold salts (e.g. sodium aurothiomalate) D- penicillamine 16

b-immunosuppressive agents Methotrexate Azathioprine Leflunomide Ciclosporine 17

Methotrexate Methotrexate is the anchor DMARD in RA. It is usually given as a starting weekly oral dose of 7.5–10 mg and this is increased in 2.5 mg increments every 2–4 weeks until benefit occurs or toxicity is limiting. The maximum recommended dose is 25 mg. The benefits of methotrexate usually start to appear within 1–2 months but a 6-month course should be given before concluding that it has been ineffective.

The most common adverse effects nausea, vomiting and malaise within 24–48 hours . Patients who experience these can sometimes be successfully treated with subcutaneous methotrexate. Folic acid (5 mg/week) reduces the incidence of adverse effects without reducing efficacy.

c- Biological Treatment These drugs are more effective than standard DMARDs (with a faster onset of action, greater clinical efficacy and sustained benefit) but because of their cost many countries have set restrictive guidelines for their use. Current recommendations are that biological therapy should be initiated only in active RA (DAS28 > 5.1) when an adequate trial of at least two other DMARDs (including methotrexate) has failed.

1- Anti-TNF therapy (Infliximab) is the first-line biological drug in RA.Several agents are available. With the exception of infliximab, which must be prescribed with methotrexate to reduce the risk of neutralizing antibodies developing, these agents can be used as monotherapy. In clinical practice, however, most are co-prescribed with methotrexate, as this is more efficacious. The main adverse effects are serious infections and reactivation of latent tuberculosis

2- Competitively blocks binding of IL-1 to its receptor (Anakinra) 3- Monoclonal antibody that binds CD20 antigen on B-cells surface (Rituximab) 23

EXAMPLES OF COMMON USEFUL SURGICAL PROCEDURES FOR MSK DISORDERS Soft tissue release decompression Carpal tunnel(Median nerve) compression Synovectomy Joint replacement arthroplasty