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Seredjuk N. M. Miziuk V. M.
Ivano-Frankivsk, 2011
Rheumatoid Arthritis Diagnostic Criteria Pathophysiology Therapeutic Approach Disease Severity and Course
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
Psoriasis, Behcet's
Monoarticular causes RA SLE Viral infection Acute Serum Sickness Untreated Crystal-induced Vasculidities
RA
Immunology
Macrophages:
Produce cytokines Cytokines (TNF-) cause systemic features Proliferation of T cells Activation of B cells Initiates proinflammatory/jointdamaging processes
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
Clinical Presentation
Gradual onset Stiffness & Swelling Intermittent or Migratory involvement Extraarticular manifestations Myalgia, fatigue, low-grade fever, 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 Enteropathic arthritis Crystal-induced SLE
Diagnostic Criteria
Symmetric peripheral polyarthritis Stiffness >1 hour Rheumatoid nodules Laboratory features Radiographic bone erosions
Rheumatoid Nodules
Extensor surfaces
elbows
Radiology
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
Mild Disease
Arthralgias >3 inflamed joints Mild functional limitation Minimally elevated CRP No erosions/cartilage loss No extraarticular disease i.e. anemia
Moderate Disease
6-20 Inflamed joints Moderate functional limitation Elevated 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:
Hypoalbuminemia
Prognostic Features
RF & Anti-CCP antibodies Early development of multiple inflamed joints and joint erosions Severe functional limitation Female Persistent joint inflammation for >12 weeks
Staging
Early
<3 months
Established/Persistent
6-12 months
End-stage
Management
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 for poorer prognosis
Therapy
Pharmacologic Therapy
Analgesics
Disease modification
SAARD slow acting antirheumatic drugs DMARD disease modifying antirheumatic drugs
Methotrexate
Leflunomide
Inhibits dihydrooratate dehydrogenase Dec. activated T-cells Onset: rapid Efficacy: 6 weeks
Azathioprine
Disease Course
Long Remission
10%
Intermittent Disease
15-30%
Ankylosing Spondylitis
Clinical History
The patient is a 50-year-old female who is complaining of pelvic pain
AS: flat lumber spine, loss of lordosis, use hips for binding
Radiographic Findings
Ankylosis of sacroiliac joints Syndesmophytes in the lumbar spine Fusion of the interspinous ligament Arthropathy of both hips Enthesopathy of ischial tuberosity
Imaging Modalities
Radiographs are the most important for detection, diagnosis, and follow-up
MRI able to assess early cartilage abnormalities and bone marrow edema magnetic resonance imaging
Recurrent Iritis caused Synechiae (adhesions between the lens and iris)
Early Sacroiliitis
Ankylosing Spondylitis: Bamboo spine, ossification follow the contour of intervertebral discs
Differential Diagnosis
Chronic & progressive form of seronegative arthritis with axial skeleton predominance Affects 0.1-0.2% of the population 90-95% of patients are HLA-B27 positive
Male:female 4-10:1
Features cont.
juvenile onset associated with more frequent & severe hip & peripheral joint involvement
Features cont.
Progresses to include facet joints, spine, iliac crest, ischial tuberosity, greater trochanter, hips, patella, calcaneus, glenohumeral joints
Features cont.
Enthesopathy - calcification & ossification of ligaments, tendons, joint capsules at insertion into bone Erosion of subligamentous bone due to inflammatory response Fusion of interspinous ligament
Dagger sign
Features cont.
Bamboo spine
Resorption of vertebral endplates Soft tissue findings are new bone formation in outer layers of annulus fibrosis as well as chronic synovitis and capsular fibrosis
Physical Findings
Patients usually present with low back pain and stiffness, which improves with activity Decreased range of motion in lumbar spine Thoraco-cervical kyphosis (late) One-third of patients will have acute, unilateral uveitis
Other Complications
Pseudoarthrosis (Anderson lesion), cervical spine fracture, C1-C2 subluxation Peripheral joint ankylosis Restrictive lung disease, upper lobe fibrosis Aortic root dilation (20%) & murmur (2%)
Treatment
Posture training & range of motion exercises to prevent kyphosis Sleep prone or supine in firm bed, no pillow Breathing exercises NSAIDs for symptomatic relief
Gout
Gout
Gout is defined as a peripheral arthritis resulting from the deposition of sodium urate crystals in one or more joints.
Gout
Gout encompasses a group of disorders that occur alone or in combination and include hyperuricemia, attacks of acute, typically monarticular, inflammatory arthritis, tophaceous deposition of urate crystals in and around joints, interstitial deposition of urate crystals in renal parenchyma, and urolithiasis.
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.
Gout
asymptomatic hyperuricemia acute gouty arthritis interval or intercritical gout chronic or tophaceous gout
Pathophysiology
Urate saturates in plasma at 7 mg/dL Urate crystals deposits in less vascular tissue
Cartilage Tendons/ligaments
Pathophysiology
Primary gout:
Secondary gout:
Excess nucleoprotein turnover (lymphoma, leukemia) Increased cell proliferation/death (psoriasis) Rare genetic disorder
Acute attack:
Over hours frequently nocturnal Excruciating pain Swelling, redness and tenderness Podagra: classic presentation May effect knees, wrist, elbow, and rarely hips.
Destructive tophacous Much greater chance if untreated Rarely presents as a chronic
Chronic:
Diagnosis
Based on history and physical Confirmed by arthrocentesis Uric acid level non specific.
Urine collection:
<800 mg underexcertor
Microscopic Diagnosis
X-ray Acute
Soft
tissue swelling
Chronic
chronic tophaceous gouty arthritis, extensive bony erosions are noted throughout the carpal bones Sclerosis and joint-space narrowing are seen in the first metatarsophalangeal joint, as well as in the fourth interphalangeal joint .
Differential Diagnosis
Septic arthritis: must be excluded Acute Rheumatic fever Palindromic Rheumatism Psoriatic arthritis
Treatment
Acute:
Stop with response or side effect Can be used for chronic disease, increased risk for suppression
Treatment
Chronic:
Diet will decrease uric acid 1 mg/dL at best Weight loss Modification of medications
Treatment
Chronic
Probenicid: Sulfinpyrazone: toxic side effects Avoid with renal disease Consider NSAIDs to avoid exacerbation of gout
Treatment
Chronic
Prognosis
Generally good Up to 50 % progress to chronic disease if untreated. Surgical intervention may be required for tophi.
Thank you!