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Rheumatoid Arthritis

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Rheumatoid arthritis

Introduction
• Autoimmune disease that results in a chronic,
systemic inflammatory disorder that may
affect many tissues and organs, but
principally attacks synovial joints.
• Affects 1-3% of adult population
• F>M: 3 to 1
• Peak age of onset -35 and 45
Pathophysiology
Stage 1: Synovitis
- Angiogenesis, proliferation of synoviocytes and infiltration of
the subsynovial layers by inflammatory cells
- Thickening of the capsular structures, villous formation of the
synovium and a cell-rich effusion into the joints and tendon
sheaths
- Potentially reversible

Stage 2: Destruction
- Articular cartilage is eroded by proteolytic enzymes and
pannus
- Bone is eroded by pannus invasion and osteoclastic
resorption
- Tendon sheaths tenosynovitis rupture of
tendons
- Synovial effusion swelling of the joints

Stage 3: Deformity
- Articular destruction, capsular stretching and tendon
rupture  instability and deformity
- In some cases, adhesion develops between apposing
layer of pannus causing fibrous ankylosis and later
bony ankylosis
Clinical features
• Symmetrical polyarthralgia, morning stiffness,
joint swelling
• Constitutional symptoms: mild grade fever,
weakness, easy fatigability, anorexia, and weight
loss
• Later on, there may be limitation of motion due
to pain or joint destruction
• Predilection for the small joints of the hands, feet
and wrists: MP joints, PIP joints, and wrists are
first to become symptomatic
Deformities
• Hand: flexor tendon synovitis, triggering of
fingers, swan neck deformity, Z deformity,
boutonniere or button hole deformity, piano-
key movement" of the ulnar styloid
• Foot: cock-up toe deformity, Hallux valgus
(lateral deviation of toes), hammer toe, claw
toe, calcaneovalgus (eversion) of hindfoot,
pes planus
• Knee: Early- flexion deformity
Late- Triple subluxation (flexion,
posterior subluxation and external
rotation)
Popliteal (‘Baker’s’) cysts
Diagnosis
Lab Tests
• Rheumatoid Factor: Rose Waller test, present in most RA
patients (80 % of affected pts); 5% normal pts also +ve.
False +ve in- SLE, sarcoidosis, TB, syphilis, chronic liver
disease
• Anti CCP antibody (anti-cyclic citrullinated peptide
antibodies): more specific ( 95%) than RA factor.
• Synovial Fluid Analysis: joint fluid in RA is sterile & has
pleocytosis (usually PMN), incr protein, & decreased
viscosity & decreased complement
• ESR: Elevated
• C Reactive Protein: positive
• Peripheral blood smear: Normocytic normochromic
anaemia
• CBC: count normal
X ray
• Juxta-articular osteopenia (rarefaction)
• Soft tissue shadow at the level of joint
because of joint effusion or synovial
hypertrophy
• Symmetric joint space loss
• Erosion of articular margin
• Subchondral erosions and cysts
• Joint subluxation and collapse
TREATMENT
Medical Management:
1. NSAIDS
2. Oral Corticosteroids- used to alleviate intractable joint
inflammation or vasculitis
3. DMARDS
– Methotrexate: anti folate, hepatic and pulmonary
toxicity; first choice DMARD, upto 15 mg per week, add
folate to reduce toxicity
– Hydroxychloroquine: check visual acuity regularly
– Sulfasalazine (anti folate activity): orange staining of urine
– Leflunomide: inhibit the proliferation of T lymphocytes
– D-Penicillamine (modulate lymphocyte functions)
– Gold: gold salts (inhibit monocyte function), side
effects thrombocytopenia, neutropenia, or proteinuria
4. Anti-cytokine agents
– Etanercept - TNF type II receptor fused to IgG1
– Infliximab- monoclonal antibody to TNF
– Adalimumab- human antibody to TNF
5. Immunosuppressive agents
– Azathioprine
– Cyclophosphamide
– Cyclosporin A
Surgical treatment
– Synovectomy
– Arthroplasty- hip, knee, shoulder, elbow, wrist,
MCP
– Arthrodesis- wrist, PIP, MCP
– Tendon transfer & reconstructive surgery of hand
Thank you

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