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INFLAMMATORY ARTHRITIS
Rheumatoid Arthritis
• Definition – symmetric inflammatory joint condition
characterized by pannus formation, joint erosion, and
systemic inflammation
• Most common inflammatory arthritis, 1% of the
population, 2:1 female to male ratio, peak incidence
between ages 40 to 60
• Onset usually insidious over months
• Genetic factors clearly important – HLA “shared
epitope” is strongest risk factor, but also non-HLA
genes such as PTPN22, STAT4, TNFAIP3
• Environmental factors – cigarette smoking increases
both risk of disease and severity of disease, also risk in
coal miners (Kaplan syndrome)
Predisposition
Longitudinal
Course of RA
Joints Commonly Involved
Pathogenesis
• History and physical are majority of
diagnosis
– Symmetric pain and swelling in small joints of
hands, wrists, feet, ankles most common,
followed by knees, elbows, shoulders
– Morning stiffness – better with activity
– Constitutional symptoms – fatigue, even
weight loss are common, but fever is VERY
RARE
– Steady, progressive, additive onset is by far
most common presentation
Diagnosis
Patterns of Onset
Insidious 55%-65% Joint stiffness, swelling,
pain, fatigue
Acute 8%-15% Fever, weight loss, fatigue,
joint abnormalities present
but often not prominent
Intermediate 15%-20% Systemic complaints more
noticeable than insidious onset
Extra-articular features
• Rheumatoid nodules
• Pleural effusions
• Atherosclerosis (new, but probably testable)
• Scleritis
• Rheumatoid vasculitis (rare)
• Felty’s syndrome (neutropenia, splenomegaly,
recurrent infection)
• High ESR or CRP common but not required
• Rheumatoid factor positive in about 50%
– RF usually indicates more severe disease, greater likelihood
of extra-articular manifestations
• Anti-CCP antibodies - relatively new (but very clinically
useful and testable!!)
– Found in about 50% of patients without much overlap with
rheumatoid factor
– Highly sensitive – positive test almost always indicates
disease (>90% specificity for RA, even in mixed autoimmune
cohorts)
Laboratory
• Classical findings of inflammatory arthritis:
– Periarticular joint erosions
– Periarticular osteopenia
– Symmetric joint space narrowing
• Note that each of these is the opposite of OA!!
– (erosions instead of spurs, osteopenia instead of
sclerosis, and symmetric instead of asymmetric joint
narrowing)
X-ray
Joint-space narrowing and
erosion are seen in up to
two thirds of patients
within the first 2 to 5 years
of disease
Early Radiographic Progression
Rheumatoid
arthritis
erosions on
X-ray
RHEUM. ARTHRITIS - Late changes
ADVANCED JOINT CHANGES:
 Joint destruction
 Pain
 Deformity
 Instability
• Early treatment with a disease modifying drug is
standard of care
• Non-disease modifying
– NSAIDs
– Prednisone
• Disease modifying
– Methotrexate – most common first line, usually around 15-
20mg/week with daily folate 1mg/day
– Sulfasalazine, leflunomide also effective
– Biological agents such as TNF-alpha blockers, abatacept,
rituximab, and tocilizumab are all second or third line
Treatment
• Goal of treatment is clinical remission if
possible
• Control of disease prevents bone erosions and
subsequent deformity and loss of function
• All disease modifying drugs are
immunosuppressive, non-biologics have risk of
GI intolerance and hair loss, TNF blockers are
associated with re-activation of tuberculosis
and rarely an MS-like disease, other biologics
are not currently in wide use
Treatment

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Inflamatory arthritis

  • 2.
  • 3.
  • 4. Rheumatoid Arthritis • Definition – symmetric inflammatory joint condition characterized by pannus formation, joint erosion, and systemic inflammation • Most common inflammatory arthritis, 1% of the population, 2:1 female to male ratio, peak incidence between ages 40 to 60 • Onset usually insidious over months
  • 5. • Genetic factors clearly important – HLA “shared epitope” is strongest risk factor, but also non-HLA genes such as PTPN22, STAT4, TNFAIP3 • Environmental factors – cigarette smoking increases both risk of disease and severity of disease, also risk in coal miners (Kaplan syndrome) Predisposition
  • 7.
  • 9.
  • 11. • History and physical are majority of diagnosis – Symmetric pain and swelling in small joints of hands, wrists, feet, ankles most common, followed by knees, elbows, shoulders – Morning stiffness – better with activity – Constitutional symptoms – fatigue, even weight loss are common, but fever is VERY RARE – Steady, progressive, additive onset is by far most common presentation Diagnosis
  • 12.
  • 13.
  • 14. Patterns of Onset Insidious 55%-65% Joint stiffness, swelling, pain, fatigue Acute 8%-15% Fever, weight loss, fatigue, joint abnormalities present but often not prominent Intermediate 15%-20% Systemic complaints more noticeable than insidious onset
  • 15.
  • 16.
  • 17.
  • 18.
  • 19.
  • 20.
  • 21. Extra-articular features • Rheumatoid nodules • Pleural effusions • Atherosclerosis (new, but probably testable) • Scleritis • Rheumatoid vasculitis (rare) • Felty’s syndrome (neutropenia, splenomegaly, recurrent infection)
  • 22.
  • 23.
  • 24.
  • 25. • High ESR or CRP common but not required • Rheumatoid factor positive in about 50% – RF usually indicates more severe disease, greater likelihood of extra-articular manifestations • Anti-CCP antibodies - relatively new (but very clinically useful and testable!!) – Found in about 50% of patients without much overlap with rheumatoid factor – Highly sensitive – positive test almost always indicates disease (>90% specificity for RA, even in mixed autoimmune cohorts) Laboratory
  • 26. • Classical findings of inflammatory arthritis: – Periarticular joint erosions – Periarticular osteopenia – Symmetric joint space narrowing • Note that each of these is the opposite of OA!! – (erosions instead of spurs, osteopenia instead of sclerosis, and symmetric instead of asymmetric joint narrowing) X-ray
  • 27. Joint-space narrowing and erosion are seen in up to two thirds of patients within the first 2 to 5 years of disease Early Radiographic Progression
  • 29.
  • 30. RHEUM. ARTHRITIS - Late changes ADVANCED JOINT CHANGES:  Joint destruction  Pain  Deformity  Instability
  • 31. • Early treatment with a disease modifying drug is standard of care • Non-disease modifying – NSAIDs – Prednisone • Disease modifying – Methotrexate – most common first line, usually around 15- 20mg/week with daily folate 1mg/day – Sulfasalazine, leflunomide also effective – Biological agents such as TNF-alpha blockers, abatacept, rituximab, and tocilizumab are all second or third line Treatment
  • 32. • Goal of treatment is clinical remission if possible • Control of disease prevents bone erosions and subsequent deformity and loss of function • All disease modifying drugs are immunosuppressive, non-biologics have risk of GI intolerance and hair loss, TNF blockers are associated with re-activation of tuberculosis and rarely an MS-like disease, other biologics are not currently in wide use Treatment