Rheumatoid Arthritis Flashcards
Define rheumatoid arthritis.
Chronic inflammatory systemic disease characterized by symmetrical de-forming polyarthritis and extra-articular manifestations
Describe the epidemiology of rheumatoid arthritis.
Common.
Prevalence is 1% of general population.
Three times more common in females,
peak incidence at 30–50 years but well recognised in children and the elderly.
Describe the pathogenesis of rheumatoid arthritis.
Cause unknown.
Interaction between genetic factors, sex hormones and infection may trigger autoimmune process causing inflammation in joints and other organs.
Describe risk factors in getting rheumatoid arthritis.
First degree relatives of indiv with RA have higher disease frequency.
Non genetic factors play a role.
Associated with other autoimmune phenomenon (eg Reynaud’s phenomenon, Sjogren’s syndrome) and HLA DR-1 and DR-4 haplotypes.
What would a patient with Rheumatoid Arthritis complain of in their history?
Gradual (occasionally rapid) onset.
Joint pain, swelling, morning stiffness, impaired function.
Usually affects peripheral joints symmetrically (occasionally monoarticular involvement,e.g. knee).
Systemic: Fatigue, fever, weight loss.
What would you find on examination of a patient with RA?
Arthritis:
Most common sites are in the hands.
Early:
- Spindling of fingers.
- Swelling at MCP and PIP joints.
- Warm, tender joints.
- Reduction in range of movement.
Late:
- Symmetrical deforming arthropathy.
- Ulnar deviation of fingers as a result of subluxation (partial dislocation) at MCP joints.
- Radial deviation of the wrist.
- Swan neck deformity (MCP and DIP fixed flexion, PIP extension).
- Boutonniere deformity (MCP and DIP joint extension, PIP flexion).
- Z deformity of the thumb.
- Trigger finger (unable to straighten finger, tendon sheath nodule palpable),tendon rupture.
- Wasting of the small muscles of the hand,
- palmar erythema.
Rheumatoid nodules:
Firm subcutaneous nodules (e.g. on elbows, palms, over extensor tendons).
Signs of complications
What do MCP and PIP stand for?
MCP- Metacarpophalangeal joint
PAP- Proximal interphalangeal joint.
What is swan neck deformity?
MCP and DIP fixed flexion, PIP extension
What is boutonniere’s deformity?
MCP and DIP joint extension, PIP flexion
What investigations would you perform for a patient if you suspected RA?
Blood: FBC (low Hb, raised platelets), Raised ESR and CRP, rheumatoid factor (monoclonal IgM against Fc portion of IgG, present in 70% of patients and 5% normal population, associated with subcutaneous nodules and extra-articular manifestations), antinuclear antibodies (30%).
Acutely: Consider joint aspiration to exclude septic arthritis.
Joint X-ray radiography:
Soft tissue swelling,
angular deformity,
periarticular erosions andosteoporosis
What are the criteria for diagnosing RA?
American College of Rheumatology
How do you diagnose RA using the American College of Rheumatology Criteria?
Four criteria must have been present for at least 6 weeks for diagnosis.
(Criteria 2-5 must be noted by a physician)
- Morning stiffness lasting more than an hour.
- Soft tissue swelling or effusion in at least three joints.
- One swollen area in wrist, metacarpophalangeal joint or proximal interphalangeal joint
- Symmetric arthritis.
- Rheumatoid nodules
- Positive rheumatoid factor in serum.
- Radiographic changes in hands or feet consistant with rheumatoid arthritis.
How would you manage a patient with RA?
Medical:
A variety of agents are used for treating disease with immunosuppressants and biological agents conferring long-lasting benefits (disease-modifying):
-Immunosuppressants: Disease-modifying drugs such as methotrexate (a first-line agentcombined with folic acid), sulfasalazine, penicillamine, azathioprine.
May take months to work, reduce complications and slow the disease progression.
Careful monitoring is needed for side effects, e.g.
FBC (for bone marrow suppression),
LFT (for hepatitis),
U&E (for renal failure),
urinalysis (for nephrotic syndrome),
eye examination (for retinopathy and corneal deposits).
-Biological agents:
Monoclonals against TNF-a (Etanercept, Infliximab) and CD20 on the surface of B cells (Rituximab) have proven efficacy. Very expensive and used as second-line agents.
-NSAIDs: For treating pain and stiffness.
.-Steroids: Only used in severe extra-articular disease or with rapid or widespread arthritis. Intra-articular long-acting steroids into large joints (e.g.knee, shoulder) may decrease pain and joint effusions.
Disease monitoring:
Annual reviews are recommended for measuring disease activity using functional rating scales, clinical examination, radiological appearances and biochemical markers (ESR, CRP);
also useful for detecting complications of rheumatoid disease (e.g.cervical myelopathy).
Physiotherapy and occupational therapy:
Essential to maintain joint function and quality of life.
Surgery: Synovectomy, arthrodesis, arthroplasty, tendon repair joint replacement
Give possible complications of RA.
Numerous organs can be involved.
Vasculitis (of skin): Nail-fold infarcts, digital gangrene, ulcers, pyoderma gangrenosum, purpuric rash.
Lung: Pleural effusion, fibrosis, rheumatoid nodules in parenchyma, obliterative bronchioloitis.
Heart: Pericarditis, pericardial rub, myocarditis, conduction abnormalities, valvular regurgitation.
Haematological:
- Anaemia of chronic disease.
- Megaloblastic anaemia (increased demand for folic acid).
- Aplastic anaemia (from drugs).
- Haemolytic anaemia (in Feltys syndrome).
Neuromuscular: Mononeuritis multiplex, peripheral neuropathy, carpal tunnel syndrome, atlantoaxial subluxation and spinal cord compression.
Renal: Analgesic nephropathy, amyloidosis.
Eyes: Scleritis, episcleritis, scleromalacia and scleromalacia perforans
What is the prognosis for a patient with RA?
Variable.
10% severely affected after 10 years and 20% have minimal disease.
Poor prognostic factors are: being female persistent raised inflammatory markers, high-titre rheumatoid factor, extra-articular manifestations
