Rheumatoid arthritis diagnosis

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Transcript of 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