rheumatoid arthritis and osteoarthritis objectives: by the end of this lecture student should know:...
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Rheumatoid Arthritis and Osteoarthritis
• Objectives:By the end of this lecture student should know:• Pathology,• Clinical features,• Laboratory and radiologic changes • Line of management
of Rheumatoid Arthritis and Osteoarthritis
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Rheumatoid Arthritis
Systemic chronic inflammatory disease
Mainly affects synovial joints
• Variable expression
• Prevalence about 3%
• Worldwide distribution
• Female:male ratio 3:1
• Peak age of onset: 25-50 years
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Rheumatoid Arthritis
• Unknown etiology
– Genetics
– Environmental
– Possible infectious component
• Autoimmune disorder
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THE PATHOLOGY OF RA • Synovitis
Joints
Tendon sheaths
Bursae
• Nodules
• Vasculitis
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RA Is Characterised by Synovitis and Joint Destruction
NORMAL RA
Synovial membrane
Cartilage
CapsuleSynovial fluid
Inflamed synovial
membrane
Pannus
Major cell types:• T lymphocytes• macrophages
Minor cell types:• fibroblasts• plasma cells• endothelium• dendritic cells
Major cell type:• neutrophils
Adapted from Feldmann M, et al. Annu Rev Immunol. 1996;14:397-440.
Cartilage thinning
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Numerous Cellular Interactions Drive the RA Process
B cell
T cell
Antigen-presenting
cells
B cell ormacrophage
Synoviocytes
Pannus
Articularcartilage
Production of collagenase and other neutral proteases
IL-1 andTNF- Chondrocytes
Rheumatoidfactors
Soluble factors and direct cell–cell contact
Immune complexesBacterial productsIL-1, TNF-, etc
Macrophage
IL-1
HLA -DR
Arend W. Semin Arthritis Rheum. 2001;30(suppl 2):1-6.
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IL-1 and TNF- Have a Number of Overlapping Proinflammatory Effects
COX-2 = cyclo-oxygenase type 2; PGE2 = prostaglandin-E2; NO = nitric oxide
COX-2PGE2
NOAdhesion molecules
ChemokinesCollagenases
IL-6
Proinflammatory effects of IL-1
Proinflammatory effects of TNF-
TNF-Osteoclast activation
Angiogenic factors
IL-1 cell death
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Activates monocytes/
macrophages
Activates chondrocytes
Induces fibroblastproliferation
Activates osteoclasts
Inflammation Synovial pannus formation
Cartilage breakdown
Bone resorption
IL-1
IL-1 Plays a Pivotal Role in the Inflammatory and Destructive Processes of RA
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Signs and Symptoms
• Joint inflammation– Tender, warm swollen joints– Symmetrical pattern
• Pain and stiffness• Symptoms in other parts of the body
– Nodules– Anemia
• Fatigue, occasional fever, malaise
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JOINT INVOLVEMENT ON PRESENTATION OF RA
Polyarticular 75% Monoarticular 25%
Small joints Knee 50%
of hands and feet 60%
Large joints 30% Shoulder }
Wrist }
Large and Hip } 50%
Small joints 10% Ankle }
Elbow }
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Articular features seen in the Rheumatoid Hand
WRIST: PIPs:
Synovitis Synovitis
Prominent ulnar styloid Fixed flexion or extension
Subluxation and collapse of deformities
carpus (Swan neck or boutonniere
Radial deviation deformity)
MCPs: THUMBS:
Synovitis Synovitis
Ulnar deviation ‘Z’ deformity
Subluxation
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Joint Destruction
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Extra-articular manifestations
• General– fever, lymphadenopathy, weight loss, fatigue
• Dermatologic– palmar erythema, nodules, vasculitis
• Ocular– episcleritis/scleritis, scleromalacia perforans,
choroid and retinal nodules
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Extra-articular manifestations
• Cardiac– pericarditis, myocarditis, coronary vasculitis,
nodules on valves
• Neuromuscular– entrapment neuropathy, peripheral
neuropathy, mononeuritis multiplex
• Hematologic– Felty’s syndrome, large granular lymphocyte
syndrome, lymphomas
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Extra-articular manifestations
• Pulmonary– pleuritis, nodules, interstitial lung disease,
bronchiolitis obliterans, arteritis, effusions
• Others– Sjogren’s syndrome, amyloidosis
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Investigations:
• Hematology : CBC , ESR
• Biochemistry : LFT , Renal profile
• Serology : RF , Anti-CCP
• Radiography : Joints , Spines ,Chest
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The 2010 ACR / EULAR classification criteria for rheumatoid arthritis
Target population (Who should be tested?): Patients who1) have at least 1 joint with definite clinical synovitis (swelling)2) with the synovitis not better explained by another disease
Add A–D; a score of 6/10 is needed to classify patient as having definite RA
A. Joint involvement1 large joint. 02-10 large joints 11-3 small joints (with or without involvement of large joints) 24-10 small joints (with or without involvement of large joints) 33-10 joints (at least 1 small joint) 5
B. Serology (at least 1 test result is needed for classification)Negative RF and negative ACPA 0Low-positive RF or low-positive ACPA 2High-positive RF or high-positive ACPA 3
C. Acute-phase reactants (1 test result is needed for classification)Normal CRP and normal ESR 0Abnormal CRP or abnormal ESR 1
D. Duration of symptoms6 weeks 0>6 weeks 1
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Treatment Goals
• Relieve pain
• Reduce inflammation
• Prevent/slow joint damage
• Improve functioning and quality of life
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Treatment Approaches
• Lifestyle modifications
• Rest
• Physical and occupational therapy
• Medications
• Surgery
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Rationale for the Early Treatment of R.A.
•Erosions develop early in the disease course•Destruction is irreversible•Disease activity is strongly associated with joint destruction later in the disease course•Early treatment can slow down radiographic progress•Disease activity must be suppressed maximally in its early stages to prevent destruction and preserve function
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Drug Treatments
• Nonsteroidal anti-inflammatory drugs (NSAIDs)
• Disease-modifying antirheumatic drugs (DMARDs)
• Biologic response modifiers
• Corticosteroids
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Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)
Traditional NSAIDs
• Aspirin • Ibuprofen • Ketoprofen• Naproxen
COX-2 Inhibitors
• Celecoxib• Rofecoxib
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Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)
• To relieve pain and inflammation
• Use in combination with a DMARD
• Gastrointestinal side effects
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Disease-Modifying Antirheumatic Drugs (DMARDs)
• Hydroxychloroquine• Sulfasalazine• Methotrexate• Leflunomide• Gold• Azathioprine
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Disease-Modifying Antirheumatic Drugs (DMARDs)
• Control symptoms
• No immediate analgesic effects
• Can delay progression of the disease (prevent/slow joint and cartilage damage and destruction)
• Effects generally not seen until a few weeks to months
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DMARDs
• hydroxychloroquine– mild non-erosive disease– combinations– 200 mg bid– eye exams
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DMARDs
• Sulfasalazine– 1 gm bid - tid– CBC, LFTs– onset 1 - 2 months
• Methotrexate– most commonly used drug– fast acting (4-6 weeks)– po, SQ - weekly– CBC, LFTs
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Biologic Response Modifiers
• Etanercept• Infliximab• Adalimumab• Tocilizumab
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OSTEOARTHRITIS
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MULTIFACTORAL ETIOLOGY OF OA
● Joint instability
● Age
● Hormonal factors
● Trauma
● Altered biochemistry
● Inflammation
● Genetic predisposition
● ? Others
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SYMPTOMS AND SIGNS OF OA• Pain – worse on use of joint• Stiffness – mild after immobility• Loss of movement• Pain on movement/restricted range• Tenderness (articular or periarticular)• Bony swelling• Soft tissue swelling• Joint crepitus
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RADIOLOGICAL FEATURES OF OA
• Narrowing of joint space
• Osteophytosis
• Altered bone contour
• Bone sclerosis and cysts
• Periarticular calcification
• Soft-tissue swelling
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MANAGEMENT OF OSTEOARTHTITIS
• Confirm diagnosis
• Initial Therapy :
Pysiotherapy
Wt loss
Local therapy
Paracetamol
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MANAGEMENT OF OSTEOARTHTITIScont
• Second-line approach:
NSAIDS
Intra-articular therapy: steroids,hyalurinate
Opioids
?glucosamines
Arthroscopy
Surgery
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