RA Flashcards
RA define
inflammatory polyarthritis with systemic manifestations
symmetriacl polyarthritis of the peripheral joints and extra-articular structures
course of disease variable
Chronic - characterised by exacerbations and remission
Aetiology
Female: Male 2:1 Age of onset 20 - 55yrs Prevalence 0.5-1% Tissue type HLA DR4 Cause unclear - auto-immune disturbance Rheumatoid factor (RF) (immunoglobulin IgM) in serum and synovial fluid 80%
Pathology
Auto-immune disease with abnormal antibody and T-cell responses to an auto-antigen (Haynes, 2004)
Widespread inflammatory process in the synovial cells lining joint capsules and other body tissues
Generalised disorder of connective tissue affecting articular and non-articular structures
articular changes
Synovial membrane inflamed & congested with blood, T-cells, plasma cells & fibrin
Membrane forms proliferations - villi
Abnormal synovial membrane - pannus (granulation tissue) grows along joint margin
Proteolytic & lysosomal enzymes erode joint cartilage followed by the articular bone surfaces
Erosion subchondral bone
Results in joint subluxation & deformity
Excess synovial fluid effusion
Osteoclast activity results in osteoporosis
Areas adjacent to joints
Associated muscle atrophy
Deformity in RA
Knees
Flexion
Valgus deformity
Feet Lateral deviation toes Prominent MT heads plantar aspect Elbows Flexion
Cervical spine
Instability atlanto-axial joint
Risk of Upper cervical spine Subluxation
- make sure no deformity
Hands Flexion + UD MCPJ Boutonniere Flexion PIP Extension DIP Swan Neck Flexion MCPJ Hyperextension PIPJ Flexion DIPJ
Wrists
Flexion + subluxation head of ulna
Ulnar deviation
Extra-articular features of RA
Range of inflammatory processes Vasculitis Rheumatoid nodules (in subcutaneous tissue) Eye tissue inflammation (sclereitis, uveitis) Kidney disease Cardiac disease myocarditis, pericarditis, effusions Implications for Exercise prescription
Diagnosis
History Clinical findings ACR criteria Blood tests CRP and ESR assess levels of inflammation - elevated (‘inflammatory markers’) CRP better indicator in first 24hrs of ‘flare-up’ Low HB also assoc with inflammation Positive ANA (Anti- Nuclear Antibodies) X-Rays Bony erosions Joint space narrowing Bony deformity Osteopenia /Osteoporosis
ACR criteria
Morning stiffness Arthritis of 3 or more joints Arthritis of hand joints Symmetric arthritis Rheumatoid nodules Serum rheumatoid factor Radiographic changes RA present if 4 of the 7 criteria present 1-4 present for at least 6 weeks
prognosis / course of disease
Variable & Unpredictable Worse if +Rh Factor Exacerbations & remissions Function 25% independent 40% moderate impairment 25% moderate / severe disability 10% wheelchair dependent Outcomes have improved dramatically with Anti-TNF therapies
monitoring disease activity
Disease Activity Score (DAS)-28 number of tender and swollen joints (out of 28) ESR Patient’s ‘global assessment of global health' on a 10cm VAS Score range= 0-9.4 >5.1 = active disease < 3.2 =well controlled disease <2.6 = remission.
Clinical features RA
Articular
Symmetrical peripheral polyarthritis
Early involvement small joints hand + wrists
Other - cervical spine, elbow, knees, ankles, MTP
Hip & DIP often spared
Pain
At rest dull ache, with movement
Tenderness
Abnormal intra-articular pressure / sensitivity
May be aggravated by clothing / bed clothes
Swelling
Effusion
intra-articular + peri-articular swelling in soft tissues
Synovitis: hypertrophy synovial membrane and increased synovial fluid
Warmth over joints
Decreased ROM due to:
Pain
Swelling
Joint changes
Muscle atrophy
Swelling can lead to reflex inhibition
Disuse atrophy
Pain inhibition
Deformity
Acute exacerbation position of comfort
Disease progression can result in irreversible changes and permanent deformity
Boutonniere deformity
Due to interruption of the central slip of the extensor tendon, which attaches to the proximal phalanx. Patient unable to extend PIP.
swan neck deformity
Swan Neck deformity= Hyperextension of PIP, hyperflexion of DIP. Due to interruption of the lateral slips of the extensor tendon
non-articular features
Systemic disorder Fatigue weight loss malaise low grade pyrexia Anaemia - 50% Skin – thin, papery, shiny Nodules - common elbow Round + firm; Usually non-disabling Tenosynovitis Carpal tunnel syndrome Popliteal (Baker’s) cyst
Management
Aims: To maintain functional independence and QOL
Early diagnosis is essential
Early referral enables aggressive intervention with disease modifying drugs, reducing long term joint damage and disability.
Guidelines for early management (RACGP, 2009).
Management in acute and chronic stages
Patient education
Medications
Pain relief
Control inflammation
Reduce disease process
Orthopaedic surgery
medications
Analgesics – Aspirin, Paracetomol
NSAIDS - Indomethacin, ibuprofen, meloxicam
COX-1 and COX-2 inhibitors (can have gastric side-effects)
Corticosteroids – Prednisolone, hydrocortisone
DMARDS (Disease- Modifying Anti-Rheumatic Drugs)
Methotrexate (MTX)
Hydroxychloroquine (Plaquenil)
Sulphasalazine (SAS)
Anti-malarials
Biologics (Anti-TNFs)-Inflixamab, Etanercept
Opioids-Codeine, pethidine, morphine (Addictive)
Anti-TNFs
TNF is a pro-inflammatory cytokine
Released by activated monocytes, macrophages and T-lymphocytes
Promotes inflammatory responses.
Anti-TNF meds have markedly reduced inflammation and reduced radiographic progression
Number of adverse effects
Best effect when used in combination with MTX
Used for patients with high levels of disease activity (DAS-28>5.1)
Those who have failed to respond to DMARDS including MTX
physio assessment
Problems arising …multiple symptoms? Functional difficulty Symptoms body chart One joint or multiple joints ? Pain behaviour (24 hour, aggs/eases, quality of pain) Stiffness, Swelling? Crepitus, weakness etc History of onset General health –extra-articular symptoms Investigations Management to date Drug history Outcome measures: AIMS, HAQ
physio PA
Observation- gait, posture, functional difficulties
ROM
Strength
Palpation –expected findings?
Special tests – consider pathology and out-rule other pathologies
Exercise tolerance.. Consider impact on cardiac system
QoL, psychological health, fatigue
(Self-report questionnaires)
Problem list & Goals /Treatment plan
Physio aims of treatment
Reduce pain
Maintain/Improve Joint ROM
Prevent deformity
Maintain/Improve muscle strength
Modify Rx during an acute flare-up
Prevent circulatory or respiratory complications
Maintain general mobility, function and independence
Prescribe or Advise on Specialised footwear / insoles/ orthotics
exercise therapy
Mainstay of physiotherapy treatment
Aim to optimise function
ROM, Strength, joint stability, endurance
Tai-Chi, hydrotherapy, aerobic
Group vs individualised
Assoc psychological impact and less fatigue
Pain is the main barrier to exercise
Pharmacological management NB
Cochrane review demonstrated that a combination of aerobic and strength training are beneficial for RA (Hurkmans et al, 2009)
dynamic exercise programs
To assess the effectiveness and safety of short-term (< 3/12) and long-term (>3/12) dynamic exercise therapy programs (aerobic capacity and/or muscle strength training), either land or water-based, for people with RA.
Inclusion Criteria for exercise :
a) frequency at least twice weekly for > 20 minutes;
b) duration > 6 weeks;
c) aerobic exercise intensity > 55% of the maximum heart rate and/or muscle strengthening exercises starting at 30% to 50% of IRM
d) performed under supervision.
Results
8 studies (n= 475 participants)
Aerobic capacity training combined with muscle strength training is recommended as routine practice in patients with RA. Most of the studies were not long enough to tell if exercise might cause long-term joint damage
key principles of exercise for RA
- minimise pain first. Meds TENS acupuncture heat cold
- avoid uncontrolled EOR mvmt
- increase tolerance and aerobic fitness
- increase strength and ROM
- relate exercise to functional task and current limitations
- individualise dosage
- modify during flare-up: no resistance.
joint protection
AIM: Minimise pain, reduce deformity and enhance function.
Liaise with Occupational Therapy
Splinting to hand function and pain
Resting splints during acute flare
Supportive footwear +/- Foot orthoses enhance gait, reduce metatarsalgia
other interventions
Thermotherapy (heat/cold) Cold during flare-up Heat can help pain and stiffness TENS Acupuncture Psychosocial support Cognitive-behavioural approaches
surgical management
Synovectomy Osteotomy Arthroplasty Tendon repair Arthrodesis
main differences between RA and OA
1. RA inflammatory Systemic + articular No bony spurs Erosions \+ rheumatoid factor
OA is metabolic Mechanical. Articular only Bony spurs No erosions
- RA
More common in women
Younger ages
OA
More common in women
Common in older
3. A little mvmt helps both too much agg No mvmt is not good Stiffer at rest Both have pain on increased movement – mvmt encouraged
RA Fatigue more common with RA Could get crepitus in advanced disease (swelling could give crepitus) Stiffness duration – 1 hour morning \+++ swelling Non articular symptoms – eyes
OA - Fatigue is less of a symtpom Crepitus in OA Stiffness in the morning < 30 mins Minimal swelling Articular symptoms only
4. RA Skin shiny ESR CRP are increased Joint erosions More obvious swelling Deformity?
OA ESR CRP normal Joint space narrowing + osteophytes Minimal swelling Deformity ?
5. RA Drugs – anti- Antiinflammatory drugs Physio – flare ups Multijoint and CV system
OA
Limited benefit of drugs – even paracetamol
Physio – weight mgmt
Single joint or multi
