Rheumatoid arthritis

Question 1

definition

Answer 1

chronic systemic inflammatory disease
deforming peripheral polyarthritis
peak onset 5th-6th decade
HLA DR4/DR1 linked (ass. w/ severity)

Question 2

presentation

Answer 2

typically:
symmetrical, swollen, painful and stiff small joints of hands and feet, worse early in the morning
can fluctuate, and larger joints may become involved

less common:
sudden onset widespread arthritis
recurring mono/polyarthropathies of various joints
persistent monoarthritis (knee, hip, shoulder)
systemic illness with extra-articular Sx

Question 3

signs

Answer 3

early (inflammation, no joint damage):
swollen MCP, PIP, wrist or MTP joints (often symmetrical)
look for tenosynovitis/bursitis

later (joint damage and deformity):
ulnar deviation of the fingers and dorsal wrist subluxation
boutonniere and swan neck deformities of fingers
z thumb
hand extensor tendons may rupture

atlanto-axial joint subluxation may rarely occur, which threatens the spinal cord

Question 4

pathophysiology

Answer 4

typified by widespread synovitis
unclear cause
production of rheumatoid factors by plasma cells in the synovium and the local formation of immune complexes plays a part
hyperplasia of the synovium causes joint damage by inhibiting nutrients and overfilling the joint space

Question 5

extra-articular signs

Answer 5

nodules - elbows and lungs
lymphadenopathy
vasculitis
fibrosing alveolitis
obliterative bronchiolitis
pleural and pericardial effusion
raynaud's
carpal tunnel
peripheral neuropathy
splenomegaly
episcleritis
scleritis
scleromalacia
osteoporosis
amyloidosis

Question 6

investigations

Answer 6

rheumatoid factor (RhF) is positive in 70%
a high titre is ass. w/ severe disease, erosions, and extra-articular disease
anti-CCP are highly specific for RA (98%)
often anaemia of chronic disease
inflammation increases platelets, CRP and ESR

Xrays - tissue swelling, juxta-articular osteopenia and decreased joint space
later there may be bony erosions, subluxation or complete carpal destruction
USS more effective than Xray at finding bone erosions and synovitis

Question 7

management

Answer 7

early referral to rheumatologist
disease activity measured by the DAS28. aim to reduce score to <3
early DMARDs and biologics
steroids rapidly reduce inflammation and Sx. useful in acute exacerbations
NSAIDs good for Sx relief
physio and occ therapy

Question 8

DMARDs

Answer 8

1st line
start within 3 months of persistent Sx
best results often achieved with a combination of methotrexate, sulfasalazine and hydroxychloroquine

Question 9

immunosuppression

Answer 9

potentially fatal SE of DMARDs
can result in pancytopenia, increased susceptibility and neutropenic sepsis

other SE:
methotrexate - pneumonitis, oral ulcers, hepatotoxicity
sulfasalazine - rash, decreased sperm count, oral ulcers
leflunomide - teratogenicity, oral ulcers, HTN, hepatotoxicity
hydroxychloroquine - irreversible retinopathy

Question 10

biological agents

Answer 10

1. TNF-alpha inhibitors:
   eg infliximab, etanercept, adalimumab
   recommended by nice if RA has failed to respond to 2 DMARDs and with DAS28 >5.1
   where methotrexate is CI, use adalimumab and etanercept as monotherapy
2. B cell depletion
   eg rituximab
   used in combo with methotrexate and approved where DMARDs and a TNFa inhibitor have failed
3. IL-1 and IL-6 inhibition
   eg toclizumab (IL-6 receptor blocker)
   used with methotrexate if anti-TNFa and rituximab have failed
4. disruption of T cell function
   eg abatercept
   used infrequently in patients with severe RA that has not responded to DMARDs, TNFa blockers or rituximab

SE of biologics:
serious infection including reactivation of TB and hep B
worsening HF
hypersensitivity
injection site reactions
blood disorders