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Dr. Müge Bıçakçıgil Kalaycı
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Second most common form of chronic arthritis
Chronic, insidious, autoimmune inflammatory disorder
Symmetric polyarthritis affecting mainly small joints in the hand and feet, as well as larger joints such as the wrist and shoulders
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Characteristic deformities include subluxations, dislocations, rheumatoid nodules, and joint contractures.
Crippling disease Shortens survival quality of life
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Twin and family studies demonstrate a heritability of 60%; approximately 30% of genetic risk is attributed to the shared epitope encoded on the human leukocyte antigen molecules.
Patients with HLA-DRB1 alleles may have a poorer prognosis
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Hormonal and reproductive factors contribute to the female excess and parity, breast feeding, and exogenous hormones are modifiers of risk.
Smoking is the strongest known environmental risk factor for RA
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The cause of rheumatoid arthritis is unknown
Genetic predisposition Enviromental event (such as infection) inappropriate self-directed immune response
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Infectious agents,Immunoregulatory and hormonal irregularities
Immune mediated chronic inflammation
Trigger:Environmental
Antigen
Genetic (30%)Self Antigen
T cell activation
Chronic InflammationLymphoid cells infiltrate synovium
New blood vessels form in synoviumSynovial proliferation
Joint destruction
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Synovial mass stretches joint capsule and ligaments: joint swelling, instability & deformity
Cytokine and proteolytic enzyme rich synovial fluid destroys cartilage joint space narrowing on X-rays
Infiltration of cartilage and later bone by invading synovium (pannus) marginal erosions
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Prevalence 0.05-0.15/1000 in developed nations.
Disease onset most common at 25-55 years of age
Incidence rises with age
Women:men 2.5:1
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The distribution of involved joint is a critical clue to the underlying diagnosis.
RA can effect any of the synovial joints.
The disease starts in the MCF, PIP,MTF joints Followed by the wrist, knees, elbows, ankles,
hips, and shoulders
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Symptoms include pain , swelling, and stiffness
Stiffness often predominating in the mornings
Early treatment helps limit the number of joints involved
RA almost always spares DIP joints
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MCP joints Synovitis Ulnar deviation
PIP joints Synovitis Swan neck deformity Boutonniere deformity
Z-deformity of thumb Tendons
Flexor tenosynovitis Extensor tenosynovitis
Poor grip: power and pinch
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Wrist
Synovitis Subluxation Radial deviation Ankylosis Carpal tunnel syndrome
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Synovitis Flexion contracture Decreased, painful pronation and
supination Olecranon bursitis RA nodules
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MTP Synovitis Subluxation with hammer toe and
metatarsalgia Toe deviation/overriding
Collapse of medial arch of foot
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Ankle Synovitis Retrocalcaneal bursitis
Tenosynovitis/rupture Peroneal tendons Tibialis posterior
Subtalar arthritis Reduced and painful movement
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Synovitis Effusions Baker’s cyst +/- rupture Instability/ deformity eg valgus
deformity Flexion contracture
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Arthritis (usually late) Pain especially on weight bearing Reduced movement
Trochanteric bursitis
SHOULDER Subacromial bursitis Rotator cuff tendinitis Glenohumeral joint arthritis Acromio-clavicular arthritis
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Involved in 70% patients with longstanding RA
Occipital pain made worse by movement
Subluxation of C1-2 with compression of spinal cord during neck flexion Significant if >10 mm instability on flexion Usually slowly developing myelopathy
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TMJ: reduced mouth opening
Sternoclavicular
Crico-arytenoid
Ossicles of ears
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Systemic features;
-fatigue, -weight loss, and -low grade fevers (≤ 38 ⁰C)
-more common in those patients with rheumatoid factor (seropositive)
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Approximately one –quarter of patients In patients who are seropositive for rheumatoid
factor.
Nodules may ocur almost anywhere lungs, heart, and eye,
Most commonly occur subcutaneously on extensor surfaces particullary forearms , over joints or pressure
points
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Firm on examination
Usually nontender( unless traumatized)
Tought to be triggered by small vessel vasculitis.
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Lungs Pleurisy Pleural effusions ( exudate!) RA nodules single/multiple (Caplan
syndrome if huge nodules in coal miners) Lung fibrosis
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RA associated small vessel vasculitis Digital infarcts Leukocytoclastic vasculitis should prompt more aggressive treatment
with disease – modifying antirheumatic drugs (DMARDs).
Pyoderma gangrenosum
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Patients with RA have significantly increased morbidity and mortality from coronary artery disease.
chronic inflammation, some of medications used, and sedantary lifestyle may be significant risk
factors.
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Pericardial effusions common (detected in up to 50 % of patients by
echocardiography) usually asymptomatic. Rarely, may result in a fibrinous pericarditis,
and constrictive pericarditis
Uncommonly, rheumatoid nodules may occur in the conduction system and cause heart block.
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Secondary Sjögren syndrome Episcleritis Scleritis Scleromalacia perforans
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Peripheral nerve entrapment syndromes Carpal tunel syndrome Tarsal tunel syndrome
Vasculitis - monoeuritis multiplex
Subluxations at C1-C2 -myelopati.
Rheumatoid nodules in the central nervous system usually asymptomatic
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The triad of RA, Splenomegaly, and Neutropenia.
In patients with severe , seropositive disease
May be accompanied by hepatomegaly, thrombocytopenia, lympadenopathy and fevers
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Most patients -do not require specific therapy
Treatment should be focused on severe RA.
Splenectomy -if severe neutropenia exists (<500 cells/µL) a
- recurrent bacterial infections
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Infections More susceptible to any infection (RA,
steroids, MTX) ESPECIALLY susceptible to joint infections
Always suspect septic arthritis if sudden increase in symptoms in one joint
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Osteoporosis and fractures RA Immobility Steroids
Amyloidosis Rare Longstanding disease Proteinuria/decreased renal function
Lymphoma
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DIAGNOSIS & EVALUATION
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Laboratory ESR/ CRP Rheumatoid factor: performed only at
baseline to establish the dx; may be repeated 6-12 ms after disease onset if negative initially
ANA Anti-CCP (anti-cyclic citrullinated
peptide)
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CBC, electrolyte, Cr, hepatic panel, U/A, : performed at baseline to assess organ dysfunction due to comorbid diseases, before starting medications
SF analysis: performed at baseline if necessary, to rule out other disease; may be repeated during disease flares to rule out septic arthritis
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Radiography Radiography of selected involved joints May have limited diagnostic value early in
the disease, but helps to establish a baseline for periodically monitoring disease progression and response to treatment
bone scan, MRI
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Post viral (parvo, rubella) Reactive arthritis SLE Polyarticular Gout Polyarticular OA
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1. Morning stiffness in and around the joints lasting at least 1 hour
2. At least 3 joint areas simultaneously have had soft tissue swelling or fluid (PIP, MCP, wrist, elbow, knee, ankle, and MTP)
3. At least 1 area swollen (as defined above) in a wrist, MCP, or PIP joint
4. Symmetical involvement of the same joint areas (as defined in 2)
5. Subcutaneous nodules over bony prominences, extensor surfaces, or in juxta-articular regions
6. Postive serum Rheumatoid Factor7. Radiographic changes typical of rheumatoid arthritis
on hand and wrist radiographs (must include erosions )
Need 4 of 7 for Diagnosis
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Joints (0-5)1 large joint 02-10 large joints 11-3 small joints (large joints not counted) 24-10 small joints (large joints not counted) 3>10 joints (at least one small joint) 5Serology (0-3)Negative RF and negative ACPAs 0Low-positive RF or low-positive ACPAs 2High-positive RF or high-positive ACPAs 3Symptom duration (0-1)<6 weeks 0≥6 weeks 1Acute-phase reactants (0-1)Normal CRP and normal ESR 0Abnormal CRP or abnormal ESR 1
ACR/EULAR 2010 CLASSIFICATION CRITERIA FOR RHEUMATOID ARTHRITIS
Cutpoint for RA: ≥ 6/10).
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RFs are human auto-Abs that react with the Fc portion of normal polyclonal IgG.
Named thus because their first description was in patients with rheumatoid arthritis
RF test is approximately 65%-75% sensitive for the diagnosis
The presence of RF, even in high titers or large amounts, is not specific for RA
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Rheumatologic Diseases Rheumatoid arthritis (~70%) Sjögren’s syndrome (~90%) Lupus (~20%) Cryoglobulinemia syndrome (90%)
Lung Diseases Interstitial fibrosis Silicosis
Infections Hepatitis C virus Acute viral infections Endocarditis Tuberculosis
Miscellaneous Sarcoidosis Malignancies Aging
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There are other RA-associated auto-Abs known to be specific for rheumatoid arthritis Perinuclear factor Antikeratin antibodies
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Early stage Soft tissue swelling
Intermediate stage Mild juxtaarticular
osteoporosis Narrowing of joint
spaceand bone erosions
Late stage Large erosions,
anatomic deformities, ankylosisBower AC. In: Klippel JH, Dieppe PA, eds. Bower AC. In: Klippel JH, Dieppe PA, eds. RheumatologyRheumatology. .
Vol 1. 2nd ed. Philadelphia, PA: WB Saunders; 1998;5:5.1–5.8.Vol 1. 2nd ed. Philadelphia, PA: WB Saunders; 1998;5:5.1–5.8.Resnick D et al. In: Kelley WN et al, eds. Resnick D et al. In: Kelley WN et al, eds. Textbook of RheumatologyTextbook of Rheumatology. 5th ed. . 5th ed. Philadelphia, PA: WB Saunders; 1997:626–685.Philadelphia, PA: WB Saunders; 1997:626–685.
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MANAGEMENT & THERAPY
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Nonpharmacologic rest
fatigue, splinting pain relief
cold, ultrasound,massage physical therapy occupational therapy Patient education
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Pharmacologic analgesics NSAIDs - full dose corticosteroids
prednisone at low dose - “bridge”, “burst” intra-articular steroids
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every patient should be considered for at least one modifying agent
limitations may not prevent damage
may not be tolerated due to toxicity
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Methotrexate Sulfasalazine Antimalarials Gold Salts Penicillamine Cyclophosphami
de Azathioprin
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hydroxychloroquine mild non-erosive disease combinations 200 mg bid eye exams
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Sulfasalazine 1 gm bid - tid CBC, LFTs onset 1 - 2 months
Methotrexate most commonly used drug fast acting (4-6 weeks) po, SQ - weekly CBC, LFTs
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Leflunomide (Arava)
Tumor Necrosing Factor InhibitorsEtanercept (Enbrel)Infliximab (Remicade)Adalimumab (Humira)
Interleukin – 1 Receptor Antagonists
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Soft tissue: Carpal tunnel release Synovectomy Tendon transfers
Joint replacement Arthodesis
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Life expectancy reduced by 7 years in men 3 years in women
Severe morbidity sudden onset do better than gradual early knee involvement bad Bad RA has a worse prognosis than
Hodgkins disease