RHEUMATOID ARTHRITIS Flashcards
What is RA?
- an chronic autoimmune inflammatory disease of synovial joints
- 1% of population
- Can be subacute (20%) (fast) or insidious (70%) (gradual)
What are the causes of RA?
Causes still unknown, thought to have some genetic factors
Describe the pathophysiology of RA
- Characterised by synovitis with thickening of the synovial lining and infiltration by inflammatory cells
- auto-antibodies RF and anti-CCP–> cell mediated defective immune response–>Immunoglobulins and cytokines present in synovial fluid–>inflammation
- synovium then proliferates and grows over articular cartilage–>tumour formation called pannus
- pannus destroys the articular cartilage and subchondral bone, producing bony erosions
What are the risk factors for RA?
- Gender: women 2-3x
- Age: 40-60 most common
- Family history
- Genetic factors (HLA-DR4 and HLA-DRB1 confer susceptibility for RA)
- Smoking
What are the signs of RA?
- 4 signs of inflammation (rubor, calor, dolor, tumour)
- Symmetrical and polyarthropathy of smaller joints
- Loss of function
- Deformity and damage
- Extra-articular involvement (15-25% of cases)
- Dorsal and lumbar spine are not involved
What are signs of deformity and damage in RA?
- Swan neck (hyperextension at PIP, flexion at DIP)
- Boutonniere (flexion at PIP, hyperextension at DIP)
- Z thumb deformity
- Ulnar deviation
- Subluxation (partial dislocation) from weakening of joint capsules causing joint instability
What are the symptoms of RA?
- Pain worse in the morning (lastings>30 min, may improve with activity)
- Morning stiffness (can be several hours in bad cases)
- General Fatigue and Malaise
What are the differential diagnoses of RA?
- OA
- SA
- Symmetrical seronegative spondyloarthropathies
- SA
- SLE
What are the investigations for RA?
- Bloods; Anaemia (normocytic, normochromic), thrombocytosis, High ESR / CRP
- Test for autoantibodies; RF and anti-CCP, ANA
- aspirate joint–>synovial fluid (exclude SA)
- X-ray
What is seen on an X-ray for RA?
- L - loss of joint space
- E - erosions (focal)
- S - soft tissue swelling
- S - soft bones (osteopaenia - send for DEXA scan)
What are the extra-articular involvement on soft tissues in RA?
- nodules (on fingers and pressure areas eg elbows)
-bursitis
tensynovitis
-muscle wasting
What are the extra-articular involvement on eyes in RA?
- Episcleritis
- Scleritis
- Necrotising scleritis
What are the extra-articular involvement on nervous system in RA?
- Mild primarily sensory peripheral neuropathy
- Legs>arms
- Entrapment neuropathies- carpal tunnel
What are the extra-articular involvement on Haematological
system in RA?
- Lymph nodes can be palpable
- Spleen may be enlarged
- Normochromic normocytic Anaemia
- Haemolytic
What are the extra-articular involvement on lungs in RA?
- Pleural effusion
- Diffuse fibrosing alveolitis
- Rheumatoid nodules
- Caplan’s syndrome (rare, coal dust exposure)
- Small airways disease
What are the extra-articular involvement on the heart in RA?
- Pericardial rub
- Pericarditis
- Pericardial effusion
Increases risk of cardiovascular disease by 2-3x (same as type 2 diabetes)
What are the extra-articular involvement on the kidneys in RA?
Amyloidosis
What are the extra-articular involvement on the skin in RA?
- Vasculitis
- ulceration
What is the goal of treatment in RA?
No treatment cures, goal: remission of symptoms, return of full function and maintenance of remission with DMARDs.
What is the non-pharmacological treatment for RA?
- Rehabilitation (improve muscle power and maintenance of mobility to prevent flexion deformities.
- Occupational therapy to find aids to reduce disability
- Smoking cessation
- Deal with depression / disability
What is the pharmacological treatment for RA?
- DMARDs (1st line treatment) eg Methotrexate, Sulfasalazine
- Biological DMARDs- TNF-alpha inhibitors eg adalimumab
- Steroids
- NSAIDS
Describe the course of DMARDs in RA
- Start within 3 months of persisting symptoms
- 6-12 weeks before benefit
- Sulfasalazine: mild to moderate disease, and is drug of choice for many, especiall younger patients and women starting a family
- Methotrexate: drug of choice for patients with more active disease. Contraindicated in pregnancy and should not be prescribed before planned conception
- Leflunomide: blocks T cell proliferation. Has similar initial response rate to sulfasalazine but improvement continues and it is better sustained at 2 years. Used alone or in combination with methotrexate
- Hydroxychloroquine, azathioprine and penicillamine used less frequently
How do DMARDs work?
- Inhibit inflammatory cytokines and thus slow development of joint erosion and irreversible damage
- Reduces cardiovascular risk
What are the S/E of methotrexate?
- mouth ulcers
- diarrhoea
- liver fibrosis
- pulmonary fibrosis
- renal impairment
What are the S/E of sulfasalazine?
- Mouth Ulcers
- Hepatitis
- Male infertility (reversible)
How do steroids work in RA?
- suppress disease activity but dose required is often large, with considerable risk of long term toxicity
- Start with oral corticosteroids
- Local injections can improve pain but repeated are avoided because they might accelerate joint damage
- IM methylprednisolone helps to control severe disease flares
How do NSAIDS work in RA?
- Effective in relieving joint pain and stiffness
- Does not slow disease progression
- Slow release preparations (eg slow-release diclofenac) can be taken at night to relieve symptoms the next day
- Paracetamol with codeine (cocodamol) or without can be added for additional pain relief
What are features which suggest poor prognosis in RA?
-insidious onset
-female sex
-increasing number of joints involved
-level of disability at onset
higher inflammatory and autoimmune markers
-signs of early erosive damage on imaging.
