RHEUMATOID ARTHRITIS


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1 : Rheumatoid Arthritis DOM MR Week of 9/8/2008 Rozina Mithani
2 : Goals General Approach to Arthritis Rheumatoid Arthritis Diagnostic Criteria Pathophysiology Therapeutic Approach Disease Severity and Course
3 : Approach to Arthritis
4 : Joint Pain most common symptom Pain (arthralgia) vs. Inflammation (arthritis) Inflammation: heat, redness, pain, swelling, loss of function inflammatory arthritis (RA, SLE) vs. pain syndrome (fibromyalgia)
5 : Number of Joints Affected Inflammatory vs. Non-Inflammatory
6 : Number of Joints Affected Monoarticular Crystal-induced Infection Reactive Arthritis Hemarthrosis OA: joint effusions Autoimmune disease Psoriasis, IBD, AS, Behçet's Oligo/Polyarticular Monoarticular causes RA SLE Viral infection B19 Acute Serum Sickness Untreated Crystal-induced Vasculidities
7 : Inflammatory vs. Non-Inflammatory Inflammatory: i.e. RA Generalized AM stiffness > 30 min Resolves with movement Classic signs of inflammation Non-Inflammatory: i.e. Osteoarthritis Localized AM stiffness < 30 min
8 :
9 : Arthrocentesis Confirm diagnoses Differentiate between inflammatory & noninflammatory Therapeutic/Adjunct to Antibiotics Labs: cell count w/diff crystal analysis Gram stain & Culture WBC >2000/µL indicates inflammatory arthritis Arthroscopy Evaluate ligamentous & cartilaginous integrity Biopsy Infectioun: aspirate thick or loculated fluid
10 : Rheumatoid Arthritis
11 : RA Systemic inflammatory autoimmune disorder ~1% of population Onset: 52 years 40-70 years of age <60 - 3-5:1 female predominance
12 : Genetics Increased incidence among Pima & Chippewa Native American tribes (5%) Genetic & Environmental HLA-DRB1*0401 & HLA-DRB1*0404 Increased risk Increased joint damage Increased joint surgery
13 : Pathophysiology
14 :
15 : Immunology Macrophages: Produce cytokines Cytokines (TNF-a) cause systemic features Release chemokines ? recruit PMNs into synovial fluid/membrane TNF-a & IL-1: Proliferation of T cells Activation of B cells Initiates proinflammatory/joint-damaging processes TH-1 cells: Mediate disease processes Activate B cells B cells: Release cytokines Plasma cells that produce Ab Osteoclasts: Bone erosion Juxta-articular & Systemic osteoporosis
16 : Pathophysiology Swelling of Synovial lining Angiogenesis Rapid division/growth of cells = Pannus Synovial thickening/hyperplasia Inflammatory vascularized tissue Generation of Metalloproteinases Cytokine release Infiltration of leukocytes Change in cell-surface adhesion molecules & cytokines Destruction of bone & cartilage
17 : Bottom Line Proliferation Destruction of joints Disability
18 : Disease Trigger Subclinical vs. Viral trigger Lab manifestations up to 10 yrs before clinical RF & anti-CCP (anti–cyclic 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
19 : Clinical Presentation Gradual onset Stiffness & Swelling Intermittent or Migratory involvement Extraarticular manifestations Myalgia, fatigue, low-grade fever, wt loss, depression
20 : Stiffness & Swelling Pain with pressure to joint Pain with movement of joint Swelling due to hypertrophy Effusion Heat Redness
21 : Physical Exam Decreased grip strength Boxing glove edema Carpal tunnel Ulnar deviation Boutonniere/Swan neck deformities Extensor tendon rupture
22 : Extraarticular Involvement Anemia Rheumatoid nodules Pleuropericarditis Neuropathy Episcleritis, Scleritis Splenomegaly Sjogren’s Vasculitis
23 : Differential Seronegative polyarthritis Psoriatic arthritis Crystal-induced Tophaceous gout Pseudogout Erosive inflammatory OA Reiter’s Enteropathic arthritis SLE Paraneoplastic syndrome
24 : Diagnostic Criteria
25 : Diagnostic Criteria Symmetric peripheral polyarthritis AM Stiffness >1 hour Rheumatoid nodules Laboratory features Radiographic bone erosions
26 : Symmetric Peripheral Polyarthritis 3 or more Joints for >6 weeks Small Joints Hands & Feet Peripheral to Proximal MCP and PIP Joints SPARES DIP MTP & Plantar subluxation Leads to Deformity & Destruction of Joints Erosion of cartilage and bone
27 : Stiffness AM or after Prolonged Inactivity Bilateral In/Around Joints > 1 hours Reflects severe joint inflammation Better with movement Present >6 weeks
28 : Rheumatoid Nodules Extensor surfaces elbows Very Specific Only occur in ~30% Late in Disease
29 : Laboratory Features RF 70-80% of pts Overlap with HCV/Cryoglobulinemia Anti-Cyclic Citrulline Peptide (anti-CCP) Rare overlap with HCV Acute Phase reactants ESR, CRP ? monitoring disease activity
30 : Rheumatoid Factor IgM against IgG IgM+ pts: more severe disease & poorer outcome Non-specific SLE, Sjögren's, Sarcoidosis, Chronic infections
31 : Anti-CCP IgG against synovial membrane peptides damaged via inflammation Value in IgM-RF negative Sensitivity (65%) & Specificity (95%) Predictive of Erosive Disease Disease severity Radiologic progression Poor functional outcomes
32 : Other Lab Abnormalities AOCD Thrombocytosis Leukocytosis ANA 30-40% Inflammatory synovial fluid Hypoalbuminemia
33 : Radiology Evaluate disease activity & joint damage Bony decalcification Baseline AP views Initiation of DMARDs
34 : Radiological Studies Plain Films Bilateral hands & feet Only 25% of lesions Less expensive Through bone cortex around joint margins Color Doppler U/S & MRI Early signs of damage i.e. Erosions Bone Edema - even with normal findings on radiography
35 :
36 :
37 : Disease Severity
38 : Arthralgias >3 inflamed joints Mild functional limitation Minimally elevated ESR & CRP No erosions/cartilage loss No extraarticular disease i.e. anemia Mild Disease
39 : Moderate Disease 6-20 Inflamed joints Moderate functional limitation Elevated ESR/CRP Radiographic evidence of inflammation No extraarticular disease
40 : 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
41 : 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
42 : CV Disease Leading cause of death ~50% 2x more likely to develop MI chronic, inflammatory vascular burden ? premature atherosclerosis MTX: elevated homocysteine levels Control inflammatory process = Decreased atherosclerosis/morbidity Lipid screening & treatment Control of obesity, Hyperhomocystinemia, DM, HTN ASA
43 : Other diseases 70% more likely to have a stroke 70% higher risk for developing infection Likely 2/2 treatment 44x more likely to develop NHL
44 : Staging Early <3 months Established/Persistent 6-12 months End-stage Significant joint destruction Functional disability
45 : Management Early and aggressive disease control Rheumatologist Referral Early/Undiagnosed: NSAIDs, short course Corticosteroids Late/Uncontrolled: DMARD therapy 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
46 : Treatment Strategies
47 : Therapy Non-Pharmacologic: Referral to PT/OT Evaluate ADLs Assistive devices/splints Weight loss Smoking cessation Pharmacologic: Anti-inflammatory Interrupt progression Development of erosions Joint space narrowing
48 : Pharmacologic Therapy Analgesics NSAIDs Glucocorticoids SAARD/DMARD Anticytokine therapy
49 : Analgesics Topical Capsaicin Diclofenac Oral Tylenol Opiods
50 : NSAIDs Pros: Analgesic, Antipyretic, Anti-inflammatory Cons: Don’t alter disease progression Ineffective in Erosive disease GI/Ulcers Hepatotoxicity Nephrotoxicity AIN Bleeding – antiplatelet Rash Aseptic meningitis
51 : Corticosteroids Decrease cytokines Slow Joint Inflammation Insomnia Emotional lability Fluid retention Weight gain HTN Hyperglycemia Osteoporosis Bisphosphonates: >5mg/d for >3months Cataracts Avascular necrosis Myopathy Psychosis
52 : Disease modification SAARD – slow acting antirheumatic drugs DMARD – disease modifying antirheumatic drugs
53 : Methotrexate Dihydrofolate reductase inhibitor Well tolerated, Mono/Combo Onset: 6-12 weeks Metabolism: Liver Clearance: Kidneys Monitoring: Baseline:CXR, PFTs, HIV, HBV/HCV CBC, LFTs Q4-8 weeks Caution with CRI Nausea Mucosal ulcerations Fatigue & Flu-like symptoms BM Toxicity Hepatotoxicity Treat with Folic acid, 1 mg/d
54 : Leflunomide Inhibits dihydrooratate dehydrogenase Dec. activated T-cells Onset: rapid Efficacy: =6 weeks Monitoring: CBC, LFTs Derm - rash, alopecia Diarrhea BM toxicity Hepatotoxicity
55 : Azathioprine Corticosteroid-sparing Monitoring: CBC Q1-2 months AST/ALT Infection BM Toxicity Hepatitis Malignancy
56 : Cyclophosphamide Alkylating agent Monitoring: CBC, UA monthly Yearly UA +/- Cytology Alopecia Nausea Infection BM suppression ? pancytopenia Infertility – pretreat women with Leuprolide Renal: hemorrhagic cystitis, bladder malignancy – treat with acrolein Oral more toxic than IV
57 : Anticytokine therapy Anti-TNF alpha agents Etanercept Infliximab Adalimumab IL-1 receptor antagonist (Anakinra)
58 : TNF-a Inhibitors Anti-inflammatory Block TNF-a (proinflammatory cytokine) Etanercept, Adalimumab (SQ), Infliximab (IV) Very expensive: > $15,000/patient Combo therapy with MTX Injection site reaction Infection Reactivated TB Infliximab infusion reaction Pancytopenia Autoantibody/SLE-like Exacerbate CHF Malignancy – lymphoma
59 : More aggressive approach Combo therapy Adjunctive therapy: TNF-a antagonist
60 : Disease Course Long Remission 10% Intermittent Disease 15-30% Progressive Disease
61 : Summary Approach to Arthritis Number of Joints Affected Inflammatory vs. Non-Inflammatory Rheumatoid Arthritis Diagnostic Criteria Pathophysiology Therapeutic Approach Disease Severity and Course
62 : Questions?

 

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