Rheumatoid Arthritis Flashcards
What is the epidemiology of RA?
F>M at 2-4:1; pre-menopausal risk = much higher
Peak of incidence is in the 40’s, but can occur at any age
What is the aetiology of RA?
Genetics:
- HLA variants DR4 and DR1 are common and associated with poor prognosis
Environmental:
- Oestrogen - as pre-menopausal risk higher in women; contraceptive pill can delay onset but not reduce the risk
- Smoking
- High birth weight
- Silica exposure
- Stress
- Alcohol abstaining
- Obesity
- DM
- Onset more common in winter
- Infection (though no causative factor identified)
What is the pathophysiology of RA?
A chronic inflammatory autoimmune disease
- Inflammation of synovial joints
- Leading to joint and periarticular tissue destruction
- Also extra-articular features
Seronegative vs seropositive for RF:
- 2/3rds are seropositive for ‘Rheumatoid Factor’ = an anti- IgG antibody (IgM/G/A) against he Fc portion of antibodies, existing to remove old IgG but something goes wrong in RA
- 1/3rd are seronegative (pathogenesis here is poorly understood)
How does RA present?
Pain and stiffness
- Worse in the morning and after rest
- Morning stiffness generally lasts <1hr
- May worsen in hot weather
Swelling
- Sometimes quite significant
- Joints may be red and hot
Pattern
- Often affects small (and large) joints on both sides of the body in a symmetrical fashion from the start
- Includes both hands, wrists, balls of feet; cervical spine, ankles, knees
- More joints are affected with the progression of the disease
Tendons
- Also have synovial linings and inflammation here can lead to rupture
Systemic symptoms
- Frequent fatigue and a general feeling of illness (+ several specific illnesses are present
Onset is relatively rapid - weeks-months
What are some specific systemic symptoms of RA?
Eye:
- Secondary Sjogren’s syndrome
- Scleritis, episcleritis
Skin:
- Leg ulcers (esp. in Felty’s syndrome = RH+ve arthritis + neutropaenia + splenomegaly)
- Rashes
- Nail fold infarcts
Rheumatoid nodules:
- Inflammatory infiltrate occurring within and near the joint capsule, are pink/red, rubbery and painless
- Can also occur in the eyes, lungs (= Caplan’s syndrome), heart and sometimes vocal cords
Neurological:
- Peripheral nerve entrapment including carpal tunnel
- Polyneuropathy
- Mononeuritis multiplex
Respiratory:
- Pleural involvement
- Pulmonary fibrosis
- Obliterative bronchiolitis
Cardiovascular:
- Pericardial involvement
- Vasculitis
- Myocardial fibrosis
- Increased MI risk
Liver:
- Mild hepatomegaly and abnormal transaminases are common
Other:
- Thyroid disorders
- Depression
- Splenomegaly
What different disease progression exist in RA?
Palindromic:
- Monoarticular attacks
- 24-48hrs
- Half will progress to another type of progression
Transient:
- Lasts <12/12 then permanently remits
- Usually seronegative
- No lasting damage
Remitting:
- Active for severeal years then remits, minimal lasting damage
Chronic, persistent:
- Most common, RH+ve or -ve - +ve have worse disease + prognosis
- Relapse/remit over course of years
Rapidly progressive:
- Over several years, severe damage, disability and complications
What are the features of joint and chronic changes on RA?
Deformity:
- Used to be more common before effective treatments
- Boutonniere deformity = PIP flexion + DIP hyperextension
- Swan-neck deformity = PIP hyperextension + DIP flexion
- Hitchhiker’s/’Z’ thumb = MCP flexion + DIP extension
- Ulnar deviation of the fingers
- Claw toe deformity = combination of one or more of MTP extension, PIP flexion, DIP flexion
Chronic changes:
- Muscle wasting
- Osteoporosis in bones near affected regions
What general investigations are indicated in RA?
ESR, CRP and plasma viscosity:
- Usually raised, may be normal
FBC:
- Normochromic, normocytic anaemia and reactive thrombocytosis are common in active disease
- Raised ferritin but low serum iron and TIBC
LFT:
- Mild elevation of alk phos and GGT
Uric acid/synovial fluid analysis:
- To exclude a polyarticular gout
- May be presence of white cells in aspirate in RA
Urinalysis:
- Microscopic haematuria/proteinuria may indicate a connective tissue disease
Antinuclear antibody:
- +ve in 30% RA (and also SLE and other related conditions)
What specific investigations are used in RA?
Rheumatoid factor:
- For those found to have synovitis on clinical examination
- 60-70% will be positive (+ 5% of the healthy population)
Anti-cyclic citrullinated peptide (anti-CCP):
- If patient is RF-ve - as this is more specific than RF in RA and may be more sensitive in errosive disease
XR hands + feet:
- Early in the course of disease with persistent synovitis in these joints
- May show: LESS = Loss of joint space, Erosions, Soft tissue swelling, Soft bones (periarticular osteopaenia)
What are the conditions of referral in suspected RA?
Urgent referral to a rheumatologist if:
- Persistent synovitis of undetermined cause with
- Small joints of hands/feet affected AND/OR
- More than one joint affected AND/OR
- Has been a delay of >3/12 between onset of symptoms and seeking medical advice
What non- drug treatments should be used in RA?
MDT care
- Patients should have access to named member of MDT coordinating their care (often a specialist nurse)
- Access to PT, OT , podiatry and psychology - should be reviewed regularly
- GP, rheumatology, PT, OT; pod, orthotistsm dieticians, pharmacists, neurologists, pain clinic, social workers, voluntary organisations
Diet:
- Mediterranean diet should be encouraged (more bread, fruit, veg, fish; less meat, replace butter + cheese with vegetable/plant oil spreads
Educational activities that promote understanding and self help
What is the mainstay of RA drug treatment?
Disease Modifying Antirheumetic Drugs (DMARDs):
- Methotrexate, sulfasalazine = 1st choices due to increased tolerance and efficacy
- Also: azathioprine, ciclosporin, d-penicillamine, hydroxychloroquine, etc.
Should be started within 6 weeks of referral with monthly monitoring until treatment target is met
Can be combined:
- Methotrexate + other DMARD + low dose corticosteroid = 1st line for newly diagnosed
- OR if people on long term treatment are not maintaining remission
What other general medications are indicated in RA?
Analgesics:
- Paracetamol, codeine etc
- Possible scope for neuropathic medicines e.g. carbamazepine or amitriptyline
NASIDs:
- Ibuprofen, diclofenac, naproxen
- Co-prescribed with PPI
- Improve signs and symptoms of RA but do nothing to disease course
COX-2 drugs:
- Celecoxib, etoricoxib
- Co-prescribe with PPI
- Similar efficacy to NSAIDs, some may be more tolerable/effective for some patients; but are more expensive
Corticosteroids:
- Low dose, used in conjunction with DMARDs for short term relief of symptoms + medium term to minimise radiological damage
- PO, IM or intra-articular
- IA injections can provide symptomatic relief pending onset of DMARDs, alleviate specific joint problems when general control is good, and be used as a monotherapy if DMARDs are inappropriate
What biological therapies are indicated in RA?
Tumour Necrosis Factor (TNF) inhibitors:
- Etanercept, infliximab, adalimumab etc
Anti-interleukin-1 therapy:
- Anakinra
T-cell co-stimulator modulator:
- Abatacept
Anti-CD20 therapy:
- Rituximab
Anti-interleukin-6 receptor therapy:
- Tocilizumab
To be started when: - Low-dose glucocorticoids, two trials of six months of traditional DMARD monotherapy or combination therapy (at least one including methotrexate) should fail to control symptoms or prevent disease progression
- A trial of a DMARD is defined as being normally of six months, with two months at standard dose, unless significant toxicity has limited the dose or duration of treatment
There are more specific guidelines for all these medications
When is surgery indicated in RA?
People who do not respond to optimal traditional management and who are affected by:
- Persistent joint pain (e.g. from damage)
- Worsening joint function
- Progressive deformity
- Persistent localised synovitis
Also for any consequences of RA:
- If imminent or actual tendon rupture
- Nerve entrapment
- Any stress fracture
