3rd year Rheumatology Lecture 3b Rheumatoid arthritis - PowerPoint PPT Presentation

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3rd year Rheumatology Lecture 3b Rheumatoid arthritis

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variable course with exacerbations and remissions of activity ... Immunopathology. Aggregates of T-cells, macrophages and plasma cells in SM. Activated phenotype ... – PowerPoint PPT presentation

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Title: 3rd year Rheumatology Lecture 3b Rheumatoid arthritis


1
3rd year RheumatologyLecture 3(b)Rheumatoid
arthritis
2
Introduction
  • RA is a common chronic inflammatory joint
    condition
  • multifactorial aetiology
  • variable course with exacerbations and remissions
    of activity
  • inflammation leads to joint damage (erosions)
  • can result in severe disability

3
History
  • Rheumatoid first used in 1859 by Garrod
  • Little evidence for RA prior to 16th Century
  • Possibly earlier in New World
  • In contrast to OA and Gout

4
Epidemiology
  • Incidence
  • 1.4/10000 male, 3.6/10000 females
  • Prevalence 0.5-2
  • malefemale 13
  • Worldwide distribution
  • higher in native Americans
  • absent in some parts of Africa
  • Onset any age but maximum
  • 40 - 70 years in women
  • 60 - 70 years in men

5
Genetic factors
  • Small increased risk in siblings
  • Monozygotic twins
  • 15 concordance
  • Dizygotic twins
  • 4 concordance
  • HLA DR4

6
Clinical features
  • Symmetrical deforming polyarthritis
  • affects synovial lining of joints, bursae and
    tendons
  • more then just joint disease
  • Presentation
  • Variable
  • Gradual or acute/subacute
  • Palindromic
  • Monoarticular
  • Symmetrical, diffuse small joint involvement

7
Progression of joint involvement
  • Spread occurs within months to years to other
    joints
  • Almost any joint may be involved
  • Spontaneous remission can occur (after acute
    onset)
  • Poor prognosis factors exist
  • Symptoms
  • Of inflammation
  • stiffness, pain, swelling, warmth, redness

8
Pattern of joint involvement
  • symmetrical
  • small joints of hands - DIP spared
  • characteristic features
  • Boutonniere
  • Swan neck
  • Z thumb
  • Volar subluxation
  • Ulnar deviation

9
Functional impairment
  • related to underlying disease activity and
  • joint damage due to previous activity

10
Extra articular disease
  • nodules
  • eye
  • lung
  • kidney
  • vasculitis
  • nerves
  • Feltys

11
Investigations
  • Haematology
  • Hb, wcc, plts, ESR
  • Biochemistry
  • UE, LFT, CRP
  • Immunology
  • RhF, ANA
  • Microbiology
  • viral titres
  • Radiology
  • XR, bone scan, MRI

12
Differential diagnosis
  • Post viral (parvo, rubella)
  • Reactive arthritis
  • SLE
  • Polyarticular Gout
  • Polyarticular OA

13
Diagnostic criteria
  • ARA 1958
  • 11 inclusion criteria
  • 7 classical RA
  • 5-6 definite RA
  • 3-4 probable RA
  • 20 exclusion criteria
  • ACR 1987 (4/7 necessary)
  • 1. Morning stiffness (gt 1 hour)
  • 2. Arthritis of at least 3 areas (gt 6 weeks)
  • 3. Arthritis of hand joints
  • 4. Symmetrical arthritis
  • 5. Rheumatoid nodules
  • 6. Serum rheumatoid factor
  • 7. Radiographic changes

14
Management
  • Education
  • Physical therapies
  • Drugs
  • analgesics
  • NSAIDs
  • DMARDs
  • Immunotherapies
  • Steroids ia, po, im, iv
  • Surgery

15
Prognosis
  • Life expectancy reduced by
  • 7 years in men
  • 3 years in women
  • Severe morbidity
  • sudden onset do better than gradual
  • early knee involvement bad
  • Bad RA has a worse prognosis than IHD or Hodgkins

16
Pathology
  • RA joint
  • SM hyperaemic, congested
  • synovial cell proliferation and villous
    hypertrophy
  • SM infiltration by lymphocytes, macrophages
  • Vascular pannus at cartilage-synovium junction
  • increased volume and cellularity of SF
  • atrophy of supporting muscles
  • osteopaenia of surrounding bone
  • Normal joint
  • synovial membrane (macrophage and fibroblast-like
    cells)
  • fibrous joint capsule
  • synovial fluid
  • cartilage covers articular surface

17
Immunopathology
  • Aggregates of T-cells, macrophages and plasma
    cells in SM
  • Activated phenotype
  • SF contains mainly neutrophils
  • Pro (TNF?, IL1, IL6) and anti-inflammatory (IL10,
    TGF?) cytokines within joint
  • Interplay between immune cells and cytokines
    generates inflammation and joint damage
  • What initiates the process and why doesnt it
    resolve?
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