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Osteoarthritis / Rheumatoid arthritis
Tim BadcockMonday, 10th March 2014
LayoutOsteoarthritisRheumatoid arthritisCase studies
OsteoarthritisDefinitionAetiologyRisk FactorsSymptoms and signsInvestigationsManagementPrognosis
DefinitionOsteoarthritis 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.
AetiologyPrimary – 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,
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
EffectsCommonly hips > knees > DIPS > PIPS > shoulders
SignsJoint swelling, gait abnormalities, warm joint, thickened skin,
widened joint (HB – Heberden, Bouchards), reduced powerXray – joint narrowing, bone cysts, subchondral sclerosis,
osteophytesOften assymetrical
SymptomsPain > stiffness after use > reduced range of motionIMPACT ON FUNCTION
InvestigationsBPSSocial – can they walk to shops, visit friends, drivePsychological – depressionBiological – bedside (goniometer, weight, height)
Bloods – FBC (CKD), U&E (NSAIDS), LFTs (ALP), ESR (rheumatoid),
Imaging – Xray, MRI joints/ligamentsSpecial test – DEXA scan
ManagementBiological – 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, NSAIDSSurgical – joint replacement (hemi/total), ligament
surgeryPsych – encourage social exercise, treat depressionSocial – encourage social activityMDT – physio, OT (opening jars), walking aids
PrognosisExcellentNot life limitingAssociated with cardiovascular disease, obesitySignificant impairment of ADLs
Rheumatoid arthritisDefinitionAetiologyRisk factorsSigns and symptomsExtra-articular manifestationsInvestigationsManagementDMARDs
DefinitionA chronic relapsing inflammatory condition of the joints
and ligaments that is characterised by joint laxity, swelling and reduction in function with additional systemic effects
FormsJuvenile idiopathic arthritis (Pauci/polyarticular)Still’s diseaseSymmetrical polyarthropathyVasculitisRhF +ve and –veFelty’sCaplan’s syndrome
AetiologyBiochemical aetiology
HLA-DR4 associationAnti-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- and IL-2/4. α
Structural aetiologyProliferation 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)
Risk factorsHLA-DR4Family historyFemaleMiddle ageInfection triggersOther autoimmune conditionsSmoking
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
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
InvestigationsBPSSocial – can they walk to shops, visit friends, drivePsychological – depressionBiological – bedside (function!!, goniometer, psoriasis)
Bloods – FBC (DMARDS), U&E (NSAIDS/Fx), LFTs (fibrosis), ESR (rheumatoid), calcium
Imaging – Xray, MRI joints/ligaments, CT chestSpecial test – RhF, anti CCP, ANA for anti-Ro and anti-La,
Biopsy
ManagementSocial – support groups, specialist nursePsychological – screen for depressionBiological – acute / chronic management
Acute – A to E approach, splinting, surgical decompressionMild = analgesia, NSAIDS, Severe = steroids, cyclophosphamide
Chronic managementConservative
stop smoking, increase exercise splintingMedical
Simple analgesia, NSAIDS (diclofenac)Steroid injectionsOral steroidsDMARDS (methotrexate, sulfasalazine, azathioprine)Monoclonal antibodies
SurgicalDecompression, osteotomy, tendon release, Arthrodesis (fusion of joints), arthroplasty
MDTPhysio, OT, GP
SteroidsEndocrine Immunological Musculoskeletal
Moon face Reactivation of TB Myopathy
Truncal obesity Infections Osteoporosis
Hirsutism Avascular necrosis
Impotence Skin
Menstrual irregularity Acne Cardiovascular
Growth suppression Striae Hypertension
Skin atrophy Congestive cardiac failure
Gastrointestinal Bruising
Peptic ulceration Impaired wound healing CNS
Pancreatitis Changes in mood and personality
Metabolic Psychosis
Ocular Sodium and fluid retention Benign intracranial hypertension
Glaucoma Hyperglycaemia
Cataracts Hyperlipoproteinemia
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- blockers e.g. Infliximab – infectionα
Case study34 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.
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 RAWhat 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?
Test before biologicsTB monospotCXRRheumatoid Arthritis Quality of Life Score (50% reduction in
symptoms)Diagnostic criteria 4/7
Morning stiffness >1 hour for > 6weeksAffecting 3+ jointsHand jointsSymmetrical arthritisRheumatoid nodulesPositive RhF or anti-CCPXray changes
Autoantibody Diagnostic AssociatedRhF Sjogren’s, Felty’s syndrome, RA
ANA SLE, Sjogrens, Systemic sclerosis
Anti-histone SLE (drug induced)
Anti-dsDNA SLE
Anti-cardiolipin Antiphospholipid synd
Anti-centromere Limited systemic sclerosis
ANA - Ro SLE, Sjogren, SS
ANA - La Sjogren
ANA – Sm SLE
ANA – Jo1 Polymyositis/dermatomyositis
ANA – Scl70/ topoisomerase 1 Diffuse SS
AMA PBC Autoimmune hepatitis
SMA Autoimmune hepatitis PBC
Anti-parietal cell Pernicious anaemia
Anti-IF Pernicious anaemia
Anti-TTG/endomysial Coeliac
Thyroid peroxidase Hashimoto Graves
Islet cell/glutamic acid decarboxylase
T1DM
Glomerular basement membrane Goodpasture’s
c-ANCA Wegener’s (GPA) Microscopic polyangitis
p-ANCA Churg-Strauss
Ach receptor Myasthenia Gravis
Case study 267 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
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