f Post graduate mcqs and discussion : Rheumatoid arthritis

Tuesday, April 3

Rheumatoid arthritis

Rheumatoid arthritis  is the most common cause of chronic inflammatory joint disease.

The most typical features are a symmetrical polyarthritis and tenosynovitis, morning stiffness, elevation of the erythrocyte sedimentation rate  and the appearance of autoantibodies that target immunoglobulins (rheumatoid factors) in the serum.

Fig : rheumatoid arthritis. 

Cause :

Important factors in the evolution of RA are:
(1) genetic susceptibility;
(2) an immunological reac￾tion, possibly involving a foreign antigen, preferen￾tially focussed on synovial tissue;
(3) an inflammatory reaction in joints and tendon sheaths;
(4) the appear￾ance of rheumatoid factors (RF) in the blood and syn￾ovium;
(5) perpetuation of the inflammatory process; and
(6) articular cartilage destruction.


Rheumatoid arthritis is a systemic disease but the most characteristic lesions are seen in the synovium or within rheumatoid nodules. The synovium is engorged with new blood vessels and packed full of inflammatory cells. It is completed in four stages :

Stage 1 – pre-clinical Well before rheumatic arthritis  becomes clinically apparent the immune pathology is already beginning. Raised ESR, C-reactive protein  and rheumatoid factors  may be detectable years before the first diagnosis.

Stage 2 – synovitis Early changes are vascular congestion with new blood vessel formation, proliferation of synoviocytes and infiltration of the subsynovial layers by polymorphs, lymphocytes and plasma cells. There is thickening of the capsular structures, villous formation of the synovium and a cell-rich effusion into the joints and tendon sheaths. Although painful, swollen and tender, these structures are still intact and mobile, and the disorder is potentially reversible.

Stage 3 – destruction Persistent inflammation causes joint and tendon destruction. Articular cartilage is eroded, partly by proteolytic enzymes, partly by vascular tissue in the folds of the synovial reflections, and partly due to direct invasion of the cartilage by a pannus of granulation tissue creeping over the articular surface. At the margins of the joint, bone is eroded by granulation tissue invasion and osteoclastic resorption. Similar changes occur in tendon sheaths, causing tenosynovitis, invasion of the collagen bundles and, eventually, partial or complete rupture of tendons. A synovial effusion, often containing copious amounts of fibrinoid material, produces swelling of the joints, tendons and bursae.

Stage 4 – deformity The combination of articular destruction, capsular stretching and tendon rupture leads to progressive instability and deformity of the joints.

Clinical features :

In the early stages, the picture is mainly that of a polysynovitis, with soft-tissue swelling and stiffness. . Another classic feature is generalized stiffness after periods of inactivity, and especially after rising from bed in the early morning. Physical signs may be minimal, but usually there is symmetrically distributed swelling and tenderness of the metacarpophalangeal joints, the proximal inter￾phalangeal joints and the wrists. Tenosynovitis is common in the extensor compartments of the wrist and the flexor sheaths of the fingers; it is diagnosed by feeling thickening, tenderness and crepitation over the back of the wrist or the palm while passively moving the fingers.

In the later stages , joint deformity becomes increasingly apparent and the acute pain of synovitis is replaced by the more constant ache of progressive joint destruction. The combination of joint instability and tendon rupture produces the typical ‘rheumatoid’ deformities: ulnar deviation of the fingers, radial and volar displacement of the wrists, valgus knees, valgus feet and clawed toes. Joint movements are restricted and often very painful.

Differential diagnosis :

Seronegative inflammatory polyarthritis
Ankylosing spondylitis
Reiter’s disease
Calcium pyrophosphate deposition disease
Lyme disease
Viral arthritis


Fixed deformities
Muscle weakness
Spinal cord compression
Systemic vasculitis
Amyloidosis .