What is a rheumatic disorder?
A generalised term which encompasses a variety of conditions which have the following in common:
• chronicity
• local and systemic manifestations of inflammation
→ chronic pain / stiffness / swelling / around joints and tendons
List the typical features of RA
• symmetrical polyarthritis
• tenosynovitis
• morning stiffness / ‘gelling’ after period of inactivity
o CF OA → takes 20-30 mins to shake off / RA 1-3 hours to shake off
• increased ESR (d/t systemic infection present!)
• appearance of anti-IgG globulins (Rheumatoid Factors).
Write brief notes on rheumatoid factor
• Most patients have increased serum Ig levels.
• 80% have a special Ig called Rheumatoid Factor (RF).
• RF is an autoantibody against the Fc portion of autologous lgG.
• RF is mainly lgM
o a. the role of RF is uncertain, its presence is correlated to the severity of RA
o b. generally patients with severe arthritis and multisystem disease usually have increased serum titres of RF.
o c. seronegative patients often have a milder form of RA.
• The nature of the underlying stimulus to RF production unknown.
• Many patients with severe Rheumatoid disease have generalised hyperplasia of lymphoid tissues
o e.g. prominent lymphadenopathy splenomegaly
• RF can be demonstrated in plasma cells in the synovium of affected joints.
• It has been postulated that:
o RF forms immune complexes with autologous lgG
o 1gG-RF complexes induce complement activation.
o Complement activation is chemotactic for neutrophils and simulations local inflammation
o RF complexes in joints and the circulation result in acute and chronic inflammatory effects in the joints and other organs.
Briefly discuss one of the theories regarding the aetiology and pathogenesis of RA
- A variety of infectious agents have been implicated in the initiation of RA: e.g. → Bacteria / Viruses / Mycoplasmas
- Bacterial cultures are usually negative.
- Epstein-Barr virus and parvoviruses may infect rheumatoid synovium, but it is not clear if this is a primary or secondary event.
- Given current knowledge it is most reasonable to suspect that:
- infectious agents initiate the disease process
What is currently believed to be the most likely theory regarding the aetiology and pathogenesis of RA?
→ Involves genetically predisposed individual
Based on current research its most reasonable to suspect that:
• infectious agents initiate the disease process
• this results in a complex series of immunological changes that are responsible for progression of the disease.
Discuss the events occurring in joints and tendons as RA progresses through its early stages to an advanced stage.
Stage 1: SYNOVITIS / EARLY
- early changes - vascular congestion
- proliferation of synoviocytes
- infiltration of the subsynovial layers by polymorphs, lymphocytes & plasma cells
→ ACUTE INFLAMMATORY RESPONSE! - Gradual thickening of the capsular structures.
- Villous formation of the synovium
- Effusion into the joints and tendon sheaths
- SSX: pain, swelling, tenderness
NB: In spite of the above all the joint structures are mobile and intact, thus the condition is potentially reversible.
Stage 2: DESTRUCTION / ESTABLISHED
- Persistent inflammation results in joint and tendon destruction
- Articular cartilage erosion is due to:
• proteolytic enzymes
• vascular tissues in the folds of the synovial reflections
• invasion of cartilage by a pannus of granulation tissue which spreads over the articular cartilage.
• Definition: the pannus is a swollen, congested and thickened synovial membrane and a proliferation of granulation tissues which contains many lymphocytes and plasma cells.- Bone erosion due to:
granulation tissues invasion
osteoclastic resorption
- Bone erosion due to:
- Tendon sheaths:
observe similar changes as in cartilage and bone.
tenosynovitis
invasion of collagen bundles by inflammatory elements causing the eventual rupture of the tendon. - Synovial effusion:
may contain: increased amounts of fibrinoid material causing swelling of joints/tendon/bursae.
Stage 3: DEFORMITY/ADVANCED (Years+++)
progressive instability and deformity of joints d/t:
articular destruction
capsular stretching
tendon rupture
Write brief notes on the rheumatoid nodule.
a. Definition: small granulomatous lesions consisting of:
• central necrotic zone
• surrounding palisade of local histiocytes
• surrounding inflammatory granulation tissue
b. Rheumatoid nodules may be found: • under the skin especially over bony prominences • in synovium • on tendons • on sclera • in viscera
List the extra-articular manifestations of RA.
1. Rheumatoid Nodules • small subcutaneous lumps • rubbery • develop in back of elbows, tendons (may rupture), viscera, eye • are pathognomonic of RA • are in 25% of RA patients
- May also observe:
- muscle wasting
- lymphadenopathy and splenomegaly
- pericarditis
- scleritis and uveitis
- nerve entrapment syndromes
- skin atrophy/ulceration
- peripheral sensory neuropathy
- Sjögren’s syndrome (autoimmune disorder disorder primarily affecting salivary & lacrimal glands)
- visceral disease
- amyloidosis
- vasculitis is present in all cases to some degree and may cause the above manifestations
- especially fingers and nail beds!
Describe the “typical” clinical presentation of RA.
- Females 30-40 years
- Complaining of pain (acute), swelling, loss of mobility in proximal joints of fingers
- Previous history of muscle pain, tiredness, weight loss, general lack of well being
Discuss the radiological manifestations in early, late and advanced RA.
- Early stages: XR’s show changes consistent with synovitis ie
- soft tissue swelling
- periarticular osteoporosis - Later stages:
- marginal bone erosions
- narrowing of articular space (esp. in the proximal joints of hands/feet). - Advanced RA:
- articular destruction
- joint deformity
- subluxation of atlanto-axial or mid cervical levels.
