AI Inflammatory Arthritis (RA, PA) Flashcards
What is rheumatoid arthritis?
- chronic systemic inflammatory disease
- characterised by symmetrical, deforming peripheral polyarthritis
- prevalence 1%
- increased in smokers, females and usually >50yrs
- HLA DR4/DR1 linked (associated w/ increased severity)
What are the clinical features of rheumatoid arthritis?
- swollen, painful joints in hands + feet
- stiffness worse in morning
- gradually gets worse w/ larger joints becoming involved
- presentation usually insidiously develops over few months
- positive ‘squeeze test’ → discomfort on squeezing across metacarpal or metatarsal joints
- may be acute onset with marked systemic disturbance
- relapsing/remiting monoarthritis of different large joints (palindromic rheumatism)
What are the late clinical signs of RA?
- swan neck + boutonnierè deformities
- ulnar deviation + subluxation of wrist and fingers
- Z-deformity of thumb
- hand extensor tendons may rupture
- larger joints can be involved later on
Extra-articular manifestations of RA affect roughly 40% of RA patients.
What are some extra-articular manifestations?
- Nodules → elbow, lungs, cardiac, CNS, lymphadenopathy, vasculitis
- Lungs → pleural disease, interstitial fibrosis, effusions
- Cardiac → IHD, pericarditis, pericardial effusion, peripheral neuropathy
- Eye → scleritis, uveitis
What is rheumatoid factor?
- IgM against your own IgG
- lots of normal people have it
- lots of people with classic rheumatoid don’t have it
- high titres associated with severe progressive disease
- but not a marker of disease activity
- detected by either Rose-Waaler test or Latex agglutination test
What are other conditions associated with a positive Rheumatoid Factor?
- Sjorgen’s syndrome (100%)
- Felty’s syndrome (100%)
- Infective endocarditis (50%)
- SLE (20-30%)
- Systemic sclerosis (30%)
- General population (5%)
- Rarely: TB, Hep B, EBV, leprosy
What is anti-CCP?
- Anti-cyclic citruillinated peptide antibody
- detectable up to 10 yrs before development of RA
- allows early detection of pts suitable for aggressive anti-TNF therapy
- similar sensitivity to RF (70%) but higher specificity (90-95%)
- NICE → pts w/ suspected RA who are RF negative should be tested for anti-CCP antibodies
NICE have stated that clinical diagnosis is more important than criteria such as those defined by the American College of Rheumatology.
What are the diagnostic criteria for a clinical diagnosis of RA?
- Those with >1 swollen joint + suggestive clinical history, which are not better explained by another disease
- Scores >6 are diagnostic
What investigations can be done for suspected rheumatoid arthritis?
- FBC, CRP → normocytic normochromic anaemia
- ESR + CRP
- U+Es, LFTs (for baseline)
- Rheumatoid factor
- Anti-CCP antibodies (if +ve, more likely to be progressive)
- X-Ray hands + feet (if erosions present at baseline, more likely to be rapidly progressive)
- Refer even if all these are negative
What are the radiographic changes in rheumatoid arthritis?
- Soft tissue swelling
- Peri-articular osteoporosis
- Absent osteophytes
- Deformity
- Erosions (later)
- Subluxation (later)
What is meant by seronegative rheumatoid?
- 1/3rd of pts are seronegative
- identical disease presentation to seropositive in most respects, but unlikely to have nodules or extra-articular features
- most have some non-classical rheumatoid factors (IgG vs IgG)
- 40% have antibodies to CCP; if so, more likely to be rapidly progressive
A number of features have been shown to predict a poor prognosis in patients with rheumatoid arthritis.
What are the poor prognostic features?
- rheumatoid factor positive
- poor functional status at presentation
- HLA DR4
- X-Ray → early erosions (eg. after <2yrs)
- extra-articular features eg. nodules
- insidious onset
- anti-CCP antibodies
- female gender
Conservative management for RA includes referring early to a rheumatologist and specialist physio and occupational therapy eg. for aids + splints.
What is the role of DMARDs in treating RA?
- start conventional DMARD monotherapy ASAP / within 3 months of persistent symptoms
- 1st-line drugs → methotrexate*, leflunomide, hydroxychloroquine + sulfasalazine
- may need “bridging treatment” with steroids
- target = remission or low disease activity
- intensive monthly monitoring until achieved
- CRP + disease activity score at each visit
- if not winning, escalate dose
- if still not winning after 6 months, step-up to dual DMARD
- if still not winning + high level of disease activity, offer biological
*monitor FBC, eGFR + LFTs every 4-6wks in first year, essential due to risk of myelosuppression and liver cirrhosis, another SE is pneumonitis
What should be done prior to commencing biological treatment?
- check tuberculin skin test or interferon gamma release assay (IGRA)
- chest radiograph
- if indicated, hep B + C and HIV serology
- treat latent TB
- warn patient that significant risk of serious infection (at least 2% per annum)
What are the biological agents for RA treatment?
-
TNF-inhibitors (commence when two DMARDs are inadequate)
- etanercept → recombinant human protein, acts as a decoy receptor for TNF-a, subcut administration, can cause demyelination, risks incl reactivation of TB
- infliximab → monoclonal antibody, binds to TNF-a + prevents it from binding w/ TNF receptors, IV admin, risks = reactivation of TB
- adalimumab → monoclonal antibody, subcut admin
- Rituximab → two 1g IV infusions given 2 weeks apart, infusion rxns common
