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Rheumatoid Arthritis

Rheumatoid arthritis is an autoimmune disease that principally attacks synovial joints, affecting 1-3% of adults. It progresses through three stages: initial synovitis and inflammation, destruction of articular cartilage and bone, and finally deformity. Clinical features include symmetrical polyarthralgia, morning stiffness, and constitutional symptoms. Diagnosis involves lab tests like rheumatoid factor, anti-CCP antibodies, and imaging of joint erosion and space narrowing. Treatment includes NSAIDs, DMARDs like methotrexate, biologics that target cytokines, immunosuppressants, and surgery for joint replacement or reconstruction in advanced cases.

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Rowsan Rijal
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201 views21 pages

Rheumatoid Arthritis

Rheumatoid arthritis is an autoimmune disease that principally attacks synovial joints, affecting 1-3% of adults. It progresses through three stages: initial synovitis and inflammation, destruction of articular cartilage and bone, and finally deformity. Clinical features include symmetrical polyarthralgia, morning stiffness, and constitutional symptoms. Diagnosis involves lab tests like rheumatoid factor, anti-CCP antibodies, and imaging of joint erosion and space narrowing. Treatment includes NSAIDs, DMARDs like methotrexate, biologics that target cytokines, immunosuppressants, and surgery for joint replacement or reconstruction in advanced cases.

Uploaded by

Rowsan Rijal
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as PPTX, PDF, TXT or read online on Scribd

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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