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Dr. Rajesh Padhi, MD,FCCP Asso Prof Internal medicine and Critical care
Goals
Approach to Arthritis
Joint Pain
(arthritis)
heat, redness, pain, swelling, loss of function inflammatory arthritis (RA, SLE) vs. pain syndrome
Monoarticular
Oligo/Polyarticular
Crystal-induced Infection Reactive Arthritis Hemarthrosis OA: joint effusions Autoimmune disease
B19
Inflammatory: i.e. RA
Generalized AM stiffness > 30 min Resolves with movement Classic signs of inflammation
Arthrocentesis
Confirm diagnoses Differentiate between inflammatory & noninflammatory Therapeutic/Adjunct to Antibiotics Labs:
cell count w/diff crystal analysis Gram stain & Culture WBC >2000/L indicates inflammatory arthritis
Arthroscopy
Evaluate ligamentous & cartilaginous integrity Biopsy Infectioun: aspirate thick or loculated fluid
Rheumatoid Arthritis
RA
Genetics
Increased incidence among Pima & Chippewa Native American tribes (5%)
Pathophysiology
Immunology
Macrophages:
Produce cytokines Cytokines (TNF-) cause systemic features Release chemokines recruit PMNs into synovial fluid/membrane
TH-1 cells:
B cells:
Osteoclasts:
Pathophysiology
Angiogenesis
Cytokine release
Infiltration of leukocytes Change in cell-surface adhesion molecules & cytokines Destruction of bone & cartilage
Bottom Line
Disease Trigger
Lab manifestations up to 10 yrs before clinical RF & anti-CCP (anticyclic citrullinated peptide) Ab Increased CRP subclinical inflammatory disease
ADLs:
> 50% of pts stop working w/i 5-10 years of disease onset ~ 80% disabled to some degree > 20 years Life expectancy: decreased by 3-18 years
Clinical Presentation
Gradual onset Stiffness & Swelling Intermittent or Migratory involvement Extraarticular manifestations Myalgia, fatigue, low-grade fever, wt loss, depression
Pain with pressure to joint Pain with movement of joint Swelling due to hypertrophy Effusion Heat Redness
Physical Exam
Decreased grip strength Boxing glove edema Carpal tunnel Ulnar deviation Boutonniere/Swan neck deformities Extensor tendon rupture
Extraarticular Involvement
Differential
Seronegative polyarthritis Erosive inflammatory OA Psoriatic arthritis Reiters Crystal-induced Enteropathic arthritis Tophaceous gout SLE Pseudogout Paraneoplastic syndrome
Diagnostic Criteria
1. Morning stiffness EMS > 1 hour 2. Arthritis of 3 joint areas 3. Arthritis of hand joints 4. Symmetric arthritis 5. Rheumatoid nodules Subcutaneous nodules over bony prominences or extensor surfaces, or in juxta-articular regions, observed by a physician 6. Serum rheumatoid factor Demonstration of abnormal amounts of serum rheumatoid factor by any method that has been positive 7. Radiographic changes Changes typical of RA on posteroanterior hand and wrist radiographs, which must include erosions or unequivocal bony decalcification localized to or most marked adjacent to the involved joints (osteoarthritis changes alone do not qualify)
Diagnostic Criteria
Symmetric peripheral polyarthritis AM Stiffness >1 hour Rheumatoid nodules Laboratory features Radiographic bone erosions
SPARES DIP
Stiffness
Rheumatoid Nodules
Extensor surfaces
elbows
Laboratory Features
RF
Rheumatoid Factor
IgM against IgG IgM+ pts: more severe disease & poorer outcome Non-specific
Anti-CCP
30-40%
Radiology
Evaluate disease activity & joint damage Bony decalcification Baseline AP views Initiation of DMARDs
Radiological Studies
Plain Films
Bilateral hands & feet Only 25% of lesions Less expensive Through bone cortex around joint margins
Early signs of damage i.e. Erosions Bone Edema - even with normal findings on radiography
Disease Severity
Mild Disease
Arthralgias >3 inflamed joints Mild functional limitation Minimally elevated ESR & CRP No erosions/cartilage loss No extraarticular disease i.e. anemia
Moderate Disease
6-20 Inflamed joints Moderate functional limitation Elevated ESR/CRP Radiographic evidence of inflammation No extraarticular disease
Severe Disease
>20 persistently inflamed joints Rapid decline in functional capacity Radiographic evidence of rapid progession of bony erosions & loss of cartilage Extraarticular disease:
AOCD, Hypoalbuminemia
Prognostic Features
RF & Anti-CCP antibodies Early development of multiple inflamed joints and joint erosions Severe functional limitation Female HLA epitope presence Lower socioeconomic status & Less education Persistent joint inflammation for >12 weeks
CV Disease
chronic, inflammatory vascular burden premature atherosclerosis MTX: elevated homocysteine levels
Lipid screening & treatment Control of obesity, Hyperhomocystinemia, DM, HTN ASA
Other diseases
70% more likely to have a stroke 70% higher risk for developing infection
Staging
Early
<3 months
Established/Persistent
6-12 months
End-stage
Management
Rheumatologist Referral
depends on the presence or absence of joint damage, functional limitation, presence of predictive factors for poorer prognosis
Goals
achieve NED & inflammation no treatment to resolve erosions once they occur
Treatment Strategies
KEY POINTS
Employ aggressive treatment with disease-modifying antirheumatic drugs Combination therapies, particularly using methotrexate as the cornerstone Biologic agents, particularly when used in combination with methotrexate, offer the greatest ability to slow structural damage
Therapy
Non-Pharmacologic:
Pharmacologic:
Referral to PT/OT Evaluate ADLs Assistive devices/splints Weight loss Smoking cessation
Pharmacologic Therapy
Analgesics
NSAIDs
Pros:
Cons:
Corticosteroids
Decrease cytokines
Insomnia Emotional lability Fluid retention Weight gain HTN Hyperglycemia Osteoporosis
Disease modification
SAARD slow acting antirheumatic drugs DMARD disease modifying antirheumatic drugs
Methotrexate
Nausea Mucosal ulcerations Fatigue & Flu-like symptoms BM Toxicity Hepatotoxicity Treat with Folic acid, 1 mg/d
Monitoring:
Baseline:CXR, PFTs, HIV, HBV/HCV CBC, LFTs Q4-8 weeks Caution with CRI
Leflunomide
Inhibits dihydrooratate dehydrogenase Dec. activated T-cells Onset: rapid Efficacy: 6 weeks
Monitoring:
CBC, LFTs
Azathioprine
Corticosteroid-sparing Monitoring:
Cyclophosphamide
Alkylating agent
Monitoring:
Alopecia Nausea Infection BM suppression pancytopenia Infertility pretreat women with Leuprolide Renal: hemorrhagic cystitis, bladder malignancy treat with acrolein Oral more toxic than IV
Anticytokine therapy
TNF-a Inhibitors
Anti-inflammatory Block TNF- (proinflammatory cytokine) Etanercept, Adalimumab (SQ), Infliximab (IV)
infusion reaction
Etanercept
First TNF alfa inhibitor S/c injection of 25 mg twice weekly or a single 50-mg injection once a week.
It is a fusion protein of the soluble portion of the human TNF p75 chain of the receptor and the fragment crystallizable (Fc) portion of human IgG1.
Infliximab
Iv 3 to 10 mg/kg. The recommended dosing regimen at weeks 0, 2, and 6, and every 8 weeks .
Adalimumab
Abatacept is a soluble, recombinant fusion protein composed of extracellular domain of cytotoxic T lymphocyteassociated antigen-4 (CTLA-4) and the modified Fc portion of IgG1
Disease Course
Long Remission
10%
Intermittent Disease
15-30%
Progressive Disease
Summary
Approach to Arthritis
Rheumatoid Arthritis
Questions?