2 rheumatoid arthritis

7/28/2019 2 Rheumatoid Arthritis

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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!

2 rheumatoid arthritis

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