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