RA Flashcards

1
Q

What is a rheumatic disorder?

A

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

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2
Q

List the typical features of RA

A

• 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).

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3
Q

Write brief notes on rheumatoid factor

A

• 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.

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4
Q

Briefly discuss one of the theories regarding the aetiology and pathogenesis of RA

A
    1. A variety of infectious agents have been implicated in the initiation of RA: e.g. → Bacteria / Viruses / Mycoplasmas
    1. Bacterial cultures are usually negative.
    1. Epstein-Barr virus and parvoviruses may infect rheumatoid synovium, but it is not clear if this is a primary or secondary event.
    1. Given current knowledge it is most reasonable to suspect that:
  • infectious agents initiate the disease process
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5
Q

What is currently believed to be the most likely theory regarding the aetiology and pathogenesis of RA?

A

→ 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.

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6
Q

Discuss the events occurring in joints and tendons as RA progresses through its early stages to an advanced stage.

A

Stage 1: SYNOVITIS / EARLY

  1. early changes - vascular congestion
    - proliferation of synoviocytes
    - infiltration of the subsynovial layers by polymorphs, lymphocytes & plasma cells
    → ACUTE INFLAMMATORY RESPONSE!
  2. Gradual thickening of the capsular structures.
  3. Villous formation of the synovium
  4. Effusion into the joints and tendon sheaths
  5. 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

  1. Persistent inflammation results in joint and tendon destruction
  2. 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.
    1. Bone erosion due to:
      granulation tissues invasion
      osteoclastic resorption
  3. 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.
  4. 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

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7
Q

Write brief notes on the rheumatoid nodule.

A

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
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8
Q

List the extra-articular manifestations of RA.

A
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
  1. 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!
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9
Q

Describe the “typical” clinical presentation of RA.

A
  • 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
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10
Q

Discuss the radiological manifestations in early, late and advanced RA.

A
  1. Early stages: XR’s show changes consistent with synovitis ie
    - soft tissue swelling
    - periarticular osteoporosis
  2. Later stages:
    - marginal bone erosions
    - narrowing of articular space (esp. in the proximal joints of hands/feet).
  3. Advanced RA:
    - articular destruction
    - joint deformity
    - subluxation of atlanto-axial or mid cervical levels.
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