rheumatoid arthritis diagnosis
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There is no singular test for diagnosing rheumatoid arthritis. Instead, rheumatoid arthritis is diagnosed based on :history & physical examination & investigations
RA is progressive, not benign.
Structural damage/disability occurs within first 2 to 3 years of disease.
Slower progression of disease linked to early treatment
The Importance of Early DiagnosisThe Importance of Early Diagnosis
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1. 6 weeks of morning stiffness > 1 hr .2. 6 weeks of swelling of three or more joints .3. 6 weeks of swelling of wrist, MCP, PIP.4. Symmetrical joint swelling. 5. X-ray changes that must include erosions or
unequivocal bony decalcification. 6. Rheumatoid nodules. 7. Positive serum rheumatoid factor.
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Can do usual activity ,discomfort or limited mobility of 1-3 joints.
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• Are made after a full medical and family history and physical and diagnostic testing.
• Medical testing may include a wide variety of tests like:-
• ESR
• CRP
• RF
• ANA (Anti nuclear antibodies)
• Joint x-rays
• MRI (Magnetic resonance imaging) & US (ultra sound)
Inflammatorymarkers
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Anti cyclic citrullinated peptide (CCP): has been found to be more specific than rheumatoid factor in rheumatoid arthritis And high titer anti-CCP may predict aggressive erosive disease
Antinuclear antibody: positive in systemic lupus erythematosus (SLE) and related conditions; also in up to 30% of rheumatoid arthritis patients and weakly positive in up to 10% of the normal population.
CONTD….
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• C-Reactive protein– Correlates with disease activity and radiologic
progression– One of the most responsive acute phase reactants– Can be elevated in many non-RA related diseases
• Erythrocyte sedimentation rate– Influenced by non-acute phase response factors– Can be elevated in many non-RA related diseases
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Is an autoantibody that is present in the blood of most people with RA (75-80%)
Directed against host immunoglobulin
(is positive in no more than 5 percent of patients without rheumatoid arthritis).
Repeat 6-12 months following disease onset if negative
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Liver function tests… mild elevation of alkaline phosphatase and .Low serum albumin .
CBC…normochromic normocytic or Microcytic anemia . Hemoglobin slightly decreased; hemoglobin averages around 10 g/dL .Platelets & WBCs Usually increased.
Urinalysis … Microscopic hematuria or proteinuria may be present, indicat connective tissue diseases.
Joint fluid … to rule out other diseases; 5,000 to 25,000 WBC with polymorphonuclear leukocytes . cultures are negative, there are no crystals, and fluid glucose level typically is low.
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X-ray change
• Loss of joint space
• Soft tissue swelling
• Bony decalcification
• Erosions
• Peri-articular osteoporosis
X-Ray of both hands and wrists and feet for suspected RA.
MRI it is more sensitive to detect RA change.
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• Social factors
– Low socioeconomic status
– Less education
– Psychosocial stress
– female sex
• Physical factors
– Extra-articular manifestations
– Elevated CRP and ESR
– High titers of RF
– early Erosions on x-ray
– Duration of disease
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• Goals of Treatment
• Relieve pain
• Reduce inflammation
• Slow down or stop joint damage
• Maintaining the ability to function in daily
activities, improving the quality of life.
• Current Treatment
• Non - pharmacological
• pharmacological
• Surgery
• Routine monitoring and ongoing care.
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• Physiotherapy is a vital part of treating RA may be useful in decreasing the symptoms of RA.
• program of exercise strengthens joints & minimize deformity and increase the range of movement and functions.
• Natural treatments include using massage with herbs, magneto therapy etc..
• Occupational therapy can give advice to do every day activities with less pain or advice on how to use splints, skills training.
• Weight loss & Smoking cessation
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•Analgesics used only for pain relief
E.g.:- Oral
Paracetamol
Topical
Capsaicin
Diclofenac
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•NSAID’s•used as an adjunct along with DMARD’s to reduce the inflammation and pain
•Effective reduction in swelling.
•Improves mobility, flexibility, range of motion
• Ineffective in Erosive diseaseNSAID’S act by inhibiting COX-1 &2 & thus reduces inflamation
- GI toxicity – ulcer -Nephrotoxicity- Hepatotoxicity -Bleeding-Aseptic meningitis
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•DMARD,s (disease modifying anti-rheumatic drugs)• used to slow down the progression of disease. E.g. Methotrexate once weekly Oral or IM & Sulfasalazine
Advantages of DMARDs •Slow disease progression
•Improve functional disability
•Decrease pain
•Interfere with inflammatory processes
•Retard development of joint erosions
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Alkylating agent .
-Alopecia -Nausea-Infertility -Infection-BM suppression (pancytopenia)-Renal: hemorrhagic cystitis, bladder malignancy
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• Combination DMARD regimen
-Does not increase toxicity levels
-long-term outcome more favorable
-Superior efficacy to single-DMARD regimen
• Possible combinations
– Methotrexate/sulfasalazine/hydroxychloroquine
– Cyclosporine/methotrexate
– Leflunomide/methotrexate
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Biologic DMARD’s genetically engineered medications that reduce inflammation and structural damage to the joints. Include: TNFα antagonists:
Adalimumab, Etanercept , Infliximab Interleukin-1 antagonist
Anakinra Suppress T-Cell activation Abatacept
Anti B-Cell monoclonal antibody Rituximab
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Anti-inflammatory block TNF-α (proinflammatory cytokine) Improves Clinical Signs & Symptoms
-Etanercept- 50mg SC weekly
-Infliximab - 3mg/kg IV
-Adalimumab - 40mg SC
-Infection -Reactivated TB-Pancytopenia -Autoantibody/SLE-like-Exacerbate CHF -Malignancy- lymphoma
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Active Hepatitis B Infection
Multiple sclerosis, optic neuritis
Active serious infections
Chronic or recurrent infections
Current neoplasia
History of TB or positive PPD (untreated)
Congestive heart failure (Class III or IV)
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Early appropriately aggressive intervention in patients with inflammatory arthritis: critical to best possible outcome.
The combination of a biologic plus MTX is frequently more effective than either agent alone.
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• 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
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Diagnosis• Establish early diagnosis of RA• Document baseline disease activity and damage• Estimate prognosis of patient
Initiate therapy• Patient education• Physical/occupational therapy• Consider NSAID and/or local or low-dose steroids• Start disease-modifying agent within 3 months
Subjective criteria
Physical exam
Laboratory tests
Radiography
Periodically assess disease activity
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Periodically assess disease activity
Inadequate response(ongoing disease activity)
Adequate response with disease activity
Methotrexate response
Methotrexate Othermonotherapy
Suboptimal methotrexate response
Combinationtherapy
Biologics
Change or add disease-modifying drugs