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Seredjuk N. M.Miziuk V. M.
Ivano-Frankivsk, 2011
Rheumatoid Arthritis
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Rheumatoid Arthritis
Diagnostic Criteria
PathophysiologyTherapeutic Approach
Disease Severity and Course
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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)
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Number of Joints Affected
Monoarticular Crystal-induced
Infection
Reactive Arthritis
Hemarthrosis
OA: joint effusions
Autoimmune disease
Psoriasis, Behcet's
Oligo/Polyarticular Monoarticular causes
RA
SLE
Viral infection
Acute Serum Sickness
Untreated Crystal-induced
Vasculidities
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RA
Systemic inflammatory autoimmune disorder ~1% of population
Onset: 52 years
40-70 years of age
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Immunology
Macrophages:
Produce cytokines Cytokines (TNF-) cause
systemic features
TNF- & 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
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Pathophysiology
Swelling of Synovial lining Angiogenesis
Rapid division/growth of cells = Pannus Synovial thickening/hyperplasia Inflammatory vascularized tissue
Cytokine release Infiltration of leukocytes Change in cell-surface adhesion molecules & cytokines Destruction of bone & cartilage
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Bottom Line
Proliferation Destruction of joints
Disability
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Disease Trigger
Subclinical vs. Viral trigger Lab manifestations up to 10 yrs before clinical
RF & anti-CCP (anticyclic citrullinated peptide) Ab
Increased CRP subclinical inflammatory disease
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Clinical Presentation
Gradual onset Stiffness & Swelling
Intermittent or Migratory involvement
Extraarticular manifestations
Myalgia, fatigue, low-grade fever,depression
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Stiffness & Swelling
Pain with pressure to joint Pain with movement of joint
Swelling due to hypertrophy
Effusion
Heat
Redness
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Physical Exam
Decreased grip strength Boxing glove edema
Carpal tunnel
Ulnar deviation
Boutonniere/Swan neck deformities
Extensor tendon rupture
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Extraarticular Involvement
Anemia
Rheumatoid nodules
Pleuropericarditis
Neuropathy
Episcleritis, Scleritis
Splenomegaly
Vasculitis
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Differential
Seronegative polyarthritis
Psoriatic arthritis
Crystal-induced
Tophaceous gout
Pseudogout
Erosive inflammatory OA
Enteropathic arthritis
SLE
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Diagnostic Criteria
Symmetric peripheral polyarthritis Stiffness >1 hour
Rheumatoid nodules
Laboratory features
Radiographic bone erosions
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Rheumatoid Nodules
Extensor surfaces elbows
Very Specific
Only occur in ~30%
Late in Disease
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Other Lab Abnormalities
Thrombocytosis Leukocytosis
Inflammatory synovial fluid
Hypoalbuminemia
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Radiology
Evaluate disease activity & joint damage Bony decalcification
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Radiological Studies
Plain Films Bilateral hands & feet
Only 25% of lesions
Less expensive
Through bone cortex around joint margins
Color Doppler & MRI (magnetic resonance imaging) Early signs of damage i.e. Erosions
Bone Edema - even with normal findings on radiography
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Arthralgias
>3 inflamed joints
Mild functional limitation
Minimally elevated CRP
No erosions/cartilage loss No extraarticular disease i.e. anemia
Mild Disease
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Moderate Disease
6-20 Inflamed joints Moderate functional limitation
Elevated CRP
Radiographic evidence of inflammation
No extraarticular disease
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Severe Disease
>20 persistently inflamed joints Rapid decline in functional capacity
Radiographic evidence of rapid progessionof bony erosions & loss of cartilage
Extraarticular disease:
Hypoalbuminemia
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Prognostic Features
RF & Anti-CCP antibodies
Early development of multiple inflamedjoints and joint erosions
Severe functional limitation
Female Persistent joint inflammation for >12
weeks
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Staging
Early
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Management
Early and aggressive disease control Rheumatologist Referral
Early/Undiagnosed: NSAIDs, short course Corticosteroids
Late/Uncontrolled:
depends on the presence or absence of joint damage,functional limitation, presence of predictive factors forpoorer prognosis
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Therapy Non-Pharmacologic:
Assistive devices
Weight loss
Smoking cessation
Pharmacologic:
Anti-inflammatory
Interrupt progression
Development oferosions
Joint space
narrowing
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Pharmacologic Therapy
Analgesics NSAIDs
Glucocorticoids
Anticytokine therapy
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Analgesics
Topical Capsaicin
Diclofenac
Oral Tylenol
Opiods
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Disease modification
SAARDslow acting antirheumatic drugs
DMARDdisease modifying antirheumatic drugs
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Methotrexate
Dihydrofolatereductase inhibitor
Well tolerated,Mono/Combo
Onset: 6-12 weeks
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Leflunomide
Inhibits dihydrooratate
dehydrogenase
Dec. activated T-cells
Onset: rapid
Efficacy: 6 weeks
Azathioprine
Cyclophosphamide
Anticytokine therapyAnti-TNF alpha agents
Etanercept
InfliximabAdalimumab
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Disease Course
Long Remission 10%
Intermittent Disease
15-30%
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Clinical History
The patient is a50-year-old female
who is complaining
of pelvic pain
Ankylosing Spondylitis
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AS: flat lumberspine, loss of
lordosis, usehips for binding
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Radiographic Findings
Ankylosis of sacroiliac joints Syndesmophytes in the lumbar spine
Fusion of the interspinous ligament
Arthropathy of both hips
Enthesopathy of ischial tuberosity
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Imaging Modalities
Radiographs are the most important fordetection, diagnosis, and follow-up
limited in early sacroiliac changes
MRI able to assess early cartilage
abnormalities and bone marrow edemamagnetic resonance imaging
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Recurrent Iritis causedSynechiae (adhesions betweenthe lens and iris)
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Early Sacroiliitis
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Advanced Sacroiliitis, Fused SIjoints
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Syndesmophytes, apophyseal jointfusion, disc peripheral ossification
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Left: squaring of vertebra,Rt.: ant. longitudinal calcification
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Ankylosing Spondylitis: Bamboo spine,ossification follow the contour of
intervertebral discs
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AnkylosingSpondylitis:
calcanealspur and
erosion
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Apical fibrosis in Ankylosing
Spondylitis
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Differential Diagnosis
Gout
Psoriatic arthritis Rieters syndrome
Rheumatoid arthritis
Spondylodiskitis
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Ankylosing SpondylitisFeatures Chronic & progressive form of
seronegative arthritis with axial skeletonpredominance
Affects 0.1-0.2% of the population
90-95% of patients are HLA-B27 positive 7% of general population is positive, only 1%
of positives will develop ankylosingspondylitis
Male:female 4-10:1
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Features cont.
Age of onset 15-35 years old
juvenile onset associated with more frequent& severe hip & peripheral joint involvement
Life expectancy unaffected, although
20% morbidity most patients able to maintain a normal
lifestyle
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Features cont.
Starts with sacroiliac joints
begins with sclerosis, eventually get ankylosis
Progresses to include facet joints, spine,iliac crest, ischial tuberosity, greater
trochanter, hips, patella, calcaneus,glenohumeral joints
peripheral joint involvement in 30%
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Features cont.
Enthesopathy - calcification & ossificationof ligaments, tendons, joint capsules atinsertion into bone
Erosion of subligamentous bone due to
inflammatory response Fusion of interspinous ligament
Dagger sign
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Features cont.
Syndesmophytes - bony bridges betweenvertebrae & ossification of joint capsule
Bamboo spine
Resorption of vertebral endplates
Soft tissue findings are new boneformation in outer layers of annulusfibrosis as well as chronic synovitis andcapsular fibrosis
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Physical Findings
Patients usually present with low back
pain and stiffness, which improves withactivity
Decreased range of motion in lumbarspine
Thoraco-cervical kyphosis (late)
One-third of patients will have acute,unilateral uveitis
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Other Complications
Pseudoarthrosis (Anderson lesion),
cervical spine fracture, C1-C2 subluxation Peripheral joint ankylosis
Restrictive lung disease, upper lobefibrosis
Aortic root dilation (20%) & murmur(2%)
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Treatment
Posture training & range of motionexercises to prevent kyphosis
Sleep prone or supine in firm bed, nopillow
Breathing exercises NSAIDs for symptomatic relief
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Gout
Gout is defined as a peripheral arthritisresulting from the deposition of sodiumurate crystals in one or more joints.
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Gout
Gout encompasses a group of disordersthat occur alone or in combination andinclude hyperuricemia, attacks of acute,
typically monarticular, inflammatoryarthritis, tophaceous deposition of uratecrystals in and around joints, interstitial
deposition of urate crystals in renalparenchyma, and urolithiasis.
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Gout
Affects less than 0.5% of the population Due to familial disposition, incidence may
be as high as 80% in families affected by
disorder.
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Gout
Typical sequence involves progressionthrough:
asymptomatic hyperuricemia
acute gouty arthritis
interval or intercritical gout chronic or tophaceous gout
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Pathophysiology Urate saturates in plasma at 7 mg/dL
Urate crystals deposits in less vascular tissue Cartilage
Tendons/ligaments
There is a predilection for peripheral joint/tissue
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Pathophysiology
Primary gout: Overproducers: 10%
Under-excretors: 90%
Secondary gout: Excess nucleoprotein turnover (lymphoma,
leukemia)
Increased cell proliferation/death (psoriasis)
Rare genetic disorder
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Acute attack: Over hours frequently nocturnal
Excruciating pain
Swelling, redness and tenderness
Podagra: classic presentation May effect knees, wrist, elbow, and rarely hips.
Chronic: Destructive tophacous
Much greater chance if untreated
Rarely presents as a chronic
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Signs and Symptoms
Renal lithiasis
Uric acid nephropathy
Urate nephropathy
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Diagnosis
Based on history and physical
Confirmed by arthrocentesis
Uric acid level non specific. 30% may show normal level
Urine collection:
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X-ray
Acute Soft tissue swelling
Chronic
chronic tophaceous goutyarthritis, extensive bonyerosions are notedthroughout the carpal bones
Sclerosis and joint-spacenarrowing are seen in the first
metatarsophalangeal joint, aswell as in the fourthinterphalangeal joint .
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Differential Diagnosis
Septic arthritis: must be excluded
Acute Rheumatic fever
Palindromic Rheumatism
Psoriatic arthritis
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Treatment
Acute:
NSAIDs anti-inflammatory doses
Colchicine 0.5 mg po q2 hours, may require 6 mg.
Stop with response or side effect Can be used for chronic disease, increased risk for
suppression
Aspirate followed by administration of corticosteroids
Prednisone
Solumedrol
Opiates and Tylenol
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Treatment
Chronic:
Diet will decrease uric acid 1 mg/dL at best
Weight loss
Modification of medications
Avoid low dose ASA, diuretics, etc.
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Treatment Chronic
Probenicid:
Sulfinpyrazone: toxic side effectsAvoid with renal disease
Consider NSAIDs to avoid exacerbation of gout
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Treatment
Chronic
Indications for Allopurinol
Tophaceous deposites
Uric acid consistently >9
Impaired renal function
Consider NSAIDs to avoid exacerbation
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Prognosis
Generally good
Up to 50 % progress to chronic disease ifuntreated.
Surgical intervention may be required fortophi.
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Thank you!