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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
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
Rheumatoid Arthritis
• Unknown etiology
–Genetics
–Environmental
–Possible infectious component
• Autoimmune disorder
THE PATHOLOGY OF RA
• Synovitis
Joints
Tendon sheaths
Bursae
• Nodules
• Vasculitis
RA Is Characterised by Synovitis and
Joint Destruction
NORMAL RA
Synovial
membrane
Cartilage
Capsule
Synovial
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
Numerous Cellular Interactions Drive
the RA Process
B cell
T cell
Antigen-
presenting
cells
B cell or
macrophage
Synoviocytes
Pannus
Articular
cartilage
Production of collagenase and other
neutral proteases
IL-1 and
TNF- Chondrocytes
Rheumatoid
factors
Soluble factors
and direct
cell–cell
contact
Immune complexes
Bacterial products
IL-1, TNF-, etc
Macrophage
IL-1
Arend W. Semin Arthritis Rheum. 2001;30(suppl 2):1-6.
IL-1 and TNF- Have a Number of
Overlapping Proinflammatory Effects
COX-2 = cyclo-oxygenase type 2; PGE2 = prostaglandin-E2; NO = nitric oxide
COX-2
PGE2
NO
Adhesion molecules
Chemokines
Collagenases
IL-6
Proinflammatory
effects of IL-1
Proinflammatory
effects of TNF-
TNF-
Osteoclast
activation
Angiogenic
factors
IL-1
cell death
Activates
monocytes/
macrophages
Activates
chondrocytes
Induces fibroblast
proliferation
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
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
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 }
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
Joint Destruction
Extra-articular manifestations
• General
– fever, lymphadenopathy, weight loss, fatigue
• Dermatologic
– palmar erythema, nodules, vasculitis
• Ocular
– episcleritis/scleritis, scleromalacia perforans,
choroid and retinal nodules
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
Extra-articular manifestations
• Pulmonary
– pleuritis, nodules, interstitial lung disease,
bronchiolitis obliterans, arteritis, effusions
• Others
– Sjogren’s syndrome, amyloidosis
Investigations:
• Hematology : CBC , ESR
• Biochemistry : LFT , Renal profile
• Serology : RF , Anti-CCP
• Radiography : Joints , Spines ,Chest
The 2010 ACR / EULAR classification criteria for rheumatoid arthritis
Target population (Who should be tested?): Patients who
1) 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 involvement
1 large joint. 0
2-10 large joints 1
1-3 small joints (with or without involvement of large joints) 2
4-10 small joints (with or without involvement of large joints) 3
3-10 joints (at least 1 small joint) 5
B. Serology (at least 1 test result is needed for classification)
Negative RF and negative ACPA 0
Low-positive RF or low-positive ACPA 2
High-positive RF or high-positive ACPA 3
C. Acute-phase reactants (1 test result is needed for classification)
Normal CRP and normal ESR 0
Abnormal CRP or abnormal ESR 1
D. Duration of symptoms
6 weeks 0
>6 weeks 1
Treatment Goals
• Relieve pain
• Reduce inflammation
• Prevent/slow joint damage
• Improve functioning and quality of life
Treatment Approaches
• Lifestyle modifications
• Rest
• Physical and occupational therapy
• Medications
• Surgery
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
Drug Treatments
• Nonsteroidal anti-inflammatory drugs
(NSAIDs)
• Disease-modifying antirheumatic drugs
(DMARDs)
• Biologic response modifiers
• Corticosteroids
Nonsteroidal Anti-Inflammatory Drugs
(NSAIDs)
Traditional NSAIDs
• Aspirin
• Ibuprofen
• Ketoprofen
• Naproxen
COX-2 Inhibitors
• Celecoxib
• Rofecoxib
Nonsteroidal Anti-Inflammatory
Drugs (NSAIDs)
• To relieve pain and inflammation
• Use in combination with a DMARD
• Gastrointestinal side effects
Disease-Modifying Antirheumatic
Drugs (DMARDs)
• Hydroxychloroquine
• Sulfasalazine
• Methotrexate
• Leflunomide
• Gold
• Azathioprine
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
DMARDs
• hydroxychloroquine
– mild non-erosive disease
– combinations
– 200 mg bid
– eye exams
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
Biologic Response Modifiers
• Etanercept
• Infliximab
• Adalimumab
• Tocilizumab
OSTEOARTHRITIS
MULTIFACTORAL ETIOLOGY OF OA
● Joint instability
● Age
● Hormonal factors
● Trauma
● Altered biochemistry
● Inflammation
● Genetic predisposition
● ? Others
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
RADIOLOGICAL FEATURES OF OA
• Narrowing of joint space
• Osteophytosis
• Altered bone contour
• Bone sclerosis and cysts
• Periarticular calcification
• Soft-tissue swelling
MANAGEMENT OF OSTEOARTHTITIS
• Confirm diagnosis
• Initial Therapy :
Physiotherapy
Wt loss
Local therapy
Paracetamol
MANAGEMENT OF OSTEOARTHTITIS
cont
• Second-line approach:
NSAIDS
Intra-articular therapy: steroids,hyalurinate
Opioids
?glucosamines
Arthroscopy
Surgery
THANK
YOU

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L35-Rheumatoid and Osteoarthritis nursing .pptx

  • 1. 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
  • 2. 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
  • 3. Rheumatoid Arthritis • Unknown etiology –Genetics –Environmental –Possible infectious component • Autoimmune disorder
  • 4. THE PATHOLOGY OF RA • Synovitis Joints Tendon sheaths Bursae • Nodules • Vasculitis
  • 5.
  • 6. RA Is Characterised by Synovitis and Joint Destruction NORMAL RA Synovial membrane Cartilage Capsule Synovial 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
  • 7. Numerous Cellular Interactions Drive the RA Process B cell T cell Antigen- presenting cells B cell or macrophage Synoviocytes Pannus Articular cartilage Production of collagenase and other neutral proteases IL-1 and TNF- Chondrocytes Rheumatoid factors Soluble factors and direct cell–cell contact Immune complexes Bacterial products IL-1, TNF-, etc Macrophage IL-1 Arend W. Semin Arthritis Rheum. 2001;30(suppl 2):1-6.
  • 8. IL-1 and TNF- Have a Number of Overlapping Proinflammatory Effects COX-2 = cyclo-oxygenase type 2; PGE2 = prostaglandin-E2; NO = nitric oxide COX-2 PGE2 NO Adhesion molecules Chemokines Collagenases IL-6 Proinflammatory effects of IL-1 Proinflammatory effects of TNF- TNF- Osteoclast activation Angiogenic factors IL-1 cell death
  • 9. Activates monocytes/ macrophages Activates chondrocytes Induces fibroblast proliferation 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
  • 10. 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
  • 11. 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 }
  • 12. 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
  • 13.
  • 14.
  • 15.
  • 17.
  • 18. Extra-articular manifestations • General – fever, lymphadenopathy, weight loss, fatigue • Dermatologic – palmar erythema, nodules, vasculitis • Ocular – episcleritis/scleritis, scleromalacia perforans, choroid and retinal nodules
  • 19. 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
  • 20. Extra-articular manifestations • Pulmonary – pleuritis, nodules, interstitial lung disease, bronchiolitis obliterans, arteritis, effusions • Others – Sjogren’s syndrome, amyloidosis
  • 21.
  • 22.
  • 23.
  • 24.
  • 25.
  • 26.
  • 27. Investigations: • Hematology : CBC , ESR • Biochemistry : LFT , Renal profile • Serology : RF , Anti-CCP • Radiography : Joints , Spines ,Chest
  • 28.
  • 29. The 2010 ACR / EULAR classification criteria for rheumatoid arthritis Target population (Who should be tested?): Patients who 1) 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 involvement 1 large joint. 0 2-10 large joints 1 1-3 small joints (with or without involvement of large joints) 2 4-10 small joints (with or without involvement of large joints) 3 3-10 joints (at least 1 small joint) 5 B. Serology (at least 1 test result is needed for classification) Negative RF and negative ACPA 0 Low-positive RF or low-positive ACPA 2 High-positive RF or high-positive ACPA 3 C. Acute-phase reactants (1 test result is needed for classification) Normal CRP and normal ESR 0 Abnormal CRP or abnormal ESR 1 D. Duration of symptoms 6 weeks 0 >6 weeks 1
  • 30. Treatment Goals • Relieve pain • Reduce inflammation • Prevent/slow joint damage • Improve functioning and quality of life
  • 31. Treatment Approaches • Lifestyle modifications • Rest • Physical and occupational therapy • Medications • Surgery
  • 32.
  • 33. 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
  • 34. Drug Treatments • Nonsteroidal anti-inflammatory drugs (NSAIDs) • Disease-modifying antirheumatic drugs (DMARDs) • Biologic response modifiers • Corticosteroids
  • 35. Nonsteroidal Anti-Inflammatory Drugs (NSAIDs) Traditional NSAIDs • Aspirin • Ibuprofen • Ketoprofen • Naproxen COX-2 Inhibitors • Celecoxib • Rofecoxib
  • 36. Nonsteroidal Anti-Inflammatory Drugs (NSAIDs) • To relieve pain and inflammation • Use in combination with a DMARD • Gastrointestinal side effects
  • 37. Disease-Modifying Antirheumatic Drugs (DMARDs) • Hydroxychloroquine • Sulfasalazine • Methotrexate • Leflunomide • Gold • Azathioprine
  • 38. 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
  • 39. DMARDs • hydroxychloroquine – mild non-erosive disease – combinations – 200 mg bid – eye exams
  • 40. 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
  • 41. Biologic Response Modifiers • Etanercept • Infliximab • Adalimumab • Tocilizumab
  • 43.
  • 44.
  • 45. MULTIFACTORAL ETIOLOGY OF OA ● Joint instability ● Age ● Hormonal factors ● Trauma ● Altered biochemistry ● Inflammation ● Genetic predisposition ● ? Others
  • 46. 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
  • 47. RADIOLOGICAL FEATURES OF OA • Narrowing of joint space • Osteophytosis • Altered bone contour • Bone sclerosis and cysts • Periarticular calcification • Soft-tissue swelling
  • 48.
  • 49.
  • 50.
  • 51.
  • 52.
  • 53. MANAGEMENT OF OSTEOARTHTITIS • Confirm diagnosis • Initial Therapy : Physiotherapy Wt loss Local therapy Paracetamol
  • 54. MANAGEMENT OF OSTEOARTHTITIS cont • Second-line approach: NSAIDS Intra-articular therapy: steroids,hyalurinate Opioids ?glucosamines Arthroscopy Surgery