1. Tim Badcock Monday, 10 th March 2014

2. Layout Osteoarthritis Rheumatoid arthritis Case studies

3. Osteoarthritis Definition Aetiology Risk Factors Symptoms and signs Investigations Management Prognosis

4. Definition Osteoarthritis is a chronic disease of articulating joints characterised by pain, swelling and reduced range of movement. It involves the degradation of cartilage of one or more joints. Aetiology Primary – attrition of cartilage from gradual wear and tear from overuse. Associated with increased water content and reduced type 2 collagen Secondary – erosion of joints already undergoing structural change e.g. gout, RA,

5. Risk factors Unmodifiable Structural abnormality e.g. Short femur, scoliosis Age Female – thinner cartilage Achondroplasia / osteochondritis dessicans Modifiable Overweight Excessive exercise Under exercising Contributing Meniscal surgery Contralateral deformity Gout Rheumatoid arthritis Psoriasis Septic arthritis Reactive arthritis Perthes disease Ligamental laxity

6. Effects Commonly hips > knees > DIPS > PIPS > shoulders Signs Joint swelling, gait abnormalities, warm joint, thickened skin, widened joint (HB – Heberden, Bouchards), reduced power Xray – joint narrowing, bone cysts, subchondral sclerosis, osteophytes Often assymetrical Symptoms Pain > stiffness after use > reduced range of motion IMPACT ON FUNCTION

8. Investigations BPS Social – can they walk to shops, visit friends, drive Psychological – depression Biological – bedside (goniometer, weight, height) Bloods – FBC (CKD), U&E (NSAIDS), LFTs (ALP), ESR (rheumatoid), Imaging – Xray, MRI joints/ligaments Special test – DEXA scan

9. Management Biological – acute {A to E approach, an be a cause of hip fracture} Lifestyle – lose weight, regular low weight bearing exercise, stop smoking, Medical – pain management, NSAIDS Surgical – joint replacement (hemi/total), ligament surgery Psych – encourage social exercise, treat depression Social – encourage social activity MDT – physio, OT (opening jars), walking aids

11. Prognosis Excellent Not life limiting Associated with cardiovascular disease, obesity Significant impairment of ADLs

12. Rheumatoid arthritis Definition Aetiology Risk factors Signs and symptoms Extra-articular manifestations Investigations Management DMARDs

13. Definition A chronic relapsing inflammatory condition of the joints and ligaments that is characterised by joint laxity, swelling and reduction in function with additional systemic effects Forms Juvenile idiopathic arthritis (Pauci/polyarticular) Still’s disease Symmetrical polyarthropathy Vasculitis RhF +ve and –ve Felty’s Caplan’s syndrome

14. Aetiology Biochemical aetiology HLA-DR4 association Anti-cyclic citrullinated peptide (anti-CCP) RhF is IgM antibodies to circulating IgG that cause immune complexes with destruction (fast progression) RhA sufferers without RhF are seronegative often IgG to IgG complexes (slow progression). T cell activation by TNF-α and IL-2/4. Structural aetiology Proliferation of synovium to form boggy joints of pannus tissue increased vascularity and capillary permeability fibroblast erosions of cartilage and subchondral bone. Increased synovial fluid content (effusion)

15. Risk factors HLA-DR4 Family history Female Middle age Infection triggers Other autoimmune conditions Smoking

16. Signs and symptoms Signs Warm, boggy joints indicates active disease Systemic inflammation signs (pyrexia, tachycardia etc. Joint tender Muscle wasting Subluxation Subcutaneous nodules Hands – ulnar deviation, MCPs, Boutonniere, swan neck, trigger finger Stenosing tenosynovitis Carpal tunnel syndrome Feet – hammer toes, hallux valgus, MTP loss, loss of arch (pedis planus) Atlanto-axial ligament Symptoms Pain Reduced movement Stiffness (morning stiffness lasting >30mins) Joint instability Radiological DOSES deformity, osteoporosis, subluxation, effusion, swelling

17. Extra-articular Cardiology Vasculitis Pericarditis Mitral valve prolapse Respiratory Rheumatoid nodules (Caplans) pulmonary fibrosis (Felty’s) bronchiectasis pleural effusion Gastro Liver fibrosis Splenomegaly (Felty’s) Urological glomerulonephritis Neuro peripheral neuropathies (carpal tunnel syndrome) Skin rheumatoid nodules – elbows and forearms Erythema nodosum Ulceration Eyes Scleritis/episcleritis Sjogren’s syndrome Felty’s syndrome Caplan’s syndromeErythema nodosum Scleritis

18. Investigations BPS Social – can they walk to shops, visit friends, drive Psychological – depression Biological – bedside (function!!, goniometer, psoriasis) Bloods – FBC (DMARDS), U&E (NSAIDS/Fx), LFTs (fibrosis), ESR (rheumatoid), calcium Imaging – Xray, MRI joints/ligaments, CT chest Special test – RhF, anti CCP, ANA for anti-Ro and anti-La, Biopsy

19. Management Social – support groups, specialist nurse Psychological – screen for depression Biological – acute / chronic management Acute – A to E approach, splinting, surgical decompression Mild = analgesia, NSAIDS, Severe = steroids, cyclophosphamide

20. Chronic management Conservative stop smoking, increase exercise splinting Medical Simple analgesia, NSAIDS (diclofenac) Steroid injections Oral steroids DMARDS (methotrexate, sulfasalazine, azathioprine) Monoclonal antibodies Surgical Decompression, osteotomy, tendon release, Arthrodesis (fusion of joints), arthroplasty MDT Physio, OT, GP

21. Steroids EndocrineImmunological Musculoskeletal Moon faceReactivation of TBMyopathy Truncal obesityInfectionsOsteoporosis HirsutismAvascular necrosis ImpotenceSkin Menstrual irregularityAcne Cardiovascular Growth suppressionStriae Hypertension Skin atrophy Congestive cardiac failure Gastrointestinal Bruising Peptic ulcerationImpaired wound healing CNS Pancreatitis Changes in mood and personality Metabolic Psychosis Ocular Sodium and fluid retention Benign intracranial hypertension GlaucomaHyperglycaemia CataractsHyperlipoproteinemia

22. DMARDS Methotrexate (except pregnancy). Folic acid inhibitor renal impairment, lung fibrosis, bone marrow suppression, liver abnormalities Regular FBC, U&E, LFTs every 3-6 months CXR Folic acid co-prescribed Sulfasalazine (if pregnant) 5 aminosalicyclic acid inhibitor (antioxidant) Thrombocytopenia/neutropaenia, LFT derangement LFTs Azathioprine (6-mercaptopurine proanalogue, inhibit purine synthesis) neutropenia, liver toxicity, pancreatitis FBC& LFTs 6 monthly Biologics rituximab (HTN, pruritus) TNF-α blockers e.g. Infliximab – infection

23. Case study 34 year old woman comes to see you. She has a 8 week history of pain affecting the small joint of her hand. The pain is worse first thing in the morning and is associated with stiffness. It takes about 1 hour for the stiffness to improve. She has felt generally unwell over the period too. She has noticed her hands and slightly swollen. She is otherwise well and only takes the OCP. She smokes 10 cigarettes a day and drinks <14 units of alcohol per week. She works as a secretary. She is concerned that she has been late to work recently because of the disruption to her morning routine. ON examination her hands are slightly swollen over the MCP and PIP joints of both hands and are tender to palpation over these joints. There is no obvious deformity to them. She has a temp of 37.5 but has no skin changes to her elbows or scalp. Her right eye is slightly red around the cornea, but not painful.

24. What are your differentials for this lady? What investigations would you do? What Xray changes would you expect in RA? Name the typical hand changes you would see in an exam patient with RA What are the extra-articular manifestations of RA? How would you manage this patient? Name some DMARDs, give a side effect for each of them? What is the mechanism of action of the biologic agents used to treat RA? What test should be done before starting biologics? What are the diagnostic criteria for RA?

25. Test before biologics TB monospot CXR Rheumatoid Arthritis Quality of Life Score (50% reduction in symptoms) Diagnostic criteria 4/7 Morning stiffness >1 hour for > 6weeks Affecting 3+ joints Hand joints Symmetrical arthritis Rheumatoid nodules Positive RhF or anti-CCP Xray changes

26. AutoantibodyDiagnosticAssociated RhFSjogren’s, Felty’s syndrome, RA ANASLE, Sjogrens, Systemic sclerosis Anti-histoneSLE (drug induced) Anti-dsDNASLE Anti-cardiolipinAntiphospholipid synd Anti-centromereLimited systemic sclerosis ANA - RoSLE, Sjogren, SS ANA - LaSjogren ANA – SmSLE ANA – Jo1Polymyositis/dermatomyositis ANA – Scl70/ topoisomerase 1Diffuse SS AMAPBCAutoimmune hepatitis SMAAutoimmune hepatitisPBC Anti-parietal cellPernicious anaemia Anti-IFPernicious anaemia Anti-TTG/endomysialCoeliac Thyroid peroxidaseHashimotoGraves Islet cell/glutamic acid decarboxylase T1DM Glomerular basement membraneGoodpasture’s c-ANCAWegener’s (GPA)Microscopic polyangitis p-ANCAChurg-Strauss Ach receptorMyasthenia Gravis

27. Case study 2 67 year old lady come to see you as she is being increasingly troubled by pain in her hands. It mostly affect her thumbs but also the small joints of her fingers. The pain is worse towards the end of the day and after she has been gardening. She has noticed some slight swelling of her joints. The pain is helped by paracetamol when it is at its worst. She is otherwise well except for hypertension which is well controlled on amlodipine 5mg OD. She does not drink alcohol and has never smoked. She is a retired secretary. On examination her hands are not grossly deformed although she does have a mild Z shaped deformity of the thumb. They are generally tender over the PIPs and DIPs of all digits with some hard swellings. She is can do up buttons and write her name, although this causes her some discomfort. She has no skin lesions at her elbows or behind her ear

28. What are your differentials for this lady? What investigations would you like to do? What X-ray changes would you expect to find? How would you manage this lady? Describe the typical changes you would see on examinations of the hands of a patient with OA