OA & RA

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Last updated 12:24 AM on 6/2/26
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40 Terms

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What is osteoarthritis?

Degenerative joint disease involving cartilage loss and structural joint changes.

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Typical OA pain pattern

Worse with use and improved with rest.

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Typical OA stiffness pattern

Brief morning stiffness, usually under 30 minutes.

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Common OA risk factors

Age, obesity, previous joint injury, repetitive use and genetics.

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Common OA joints

Knees, hips, hands and spine.

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Pathophysiology of OA

Cartilage breakdown, subchondral bone changes and low-grade inflammation.

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OA symptoms

Pain, stiffness, reduced function, crepitus and reduced range of motion.

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OA treatment goals

Reduce pain, improve function and maintain quality of life.

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Non-drug OA management

Exercise, weight loss, education, physiotherapy and aids.

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Why is exercise recommended in OA?

Improves strength, mobility and function.

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Why is weight loss recommended in OA?

Reduces joint load and pain.

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Why are topical options useful in OA?

Lower systemic adverse effect risk.

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Nursing role in OA

Education, pain monitoring, function support and encouraging safe activity.

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How does OA differ from RA?

OA is mainly degenerative, RA is autoimmune inflammatory.

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OA prognosis

Chronic and progressive but symptoms can be managed.

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What is rheumatoid arthritis?

Chronic systemic autoimmune inflammatory disease affecting synovial joints.

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Main pathology in RA

Persistent synovitis causing joint damage.

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Typical RA joint pattern

Symmetrical small-joint involvement.

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Common RA joints

MCP, PIP, wrists, MTPs, knees and shoulders.

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Typical RA stiffness pattern

Morning stiffness often longer than one hour.

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Early RA symptoms

Fatigue, weakness, low-grade fever, joint pain and swelling.

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Later RA complications

Joint deformity, tendon destruction, ankylosis and functional limitation.

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Examples of RA deformities

Ulnar deviation, boutonnière deformity and swan-neck deformity.

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Extra-articular RA features

Nodules, lung disease, eye/mouth dryness, neuropathy and cardiovascular risk.

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RA risk factors

Genetics, smoking and environmental triggers.

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Why is smoking important in RA?

Linked to development, severity and poorer response.

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Why is early RA treatment important?

Prevents irreversible joint damage.

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Why should suspected RA be referred urgently?

Early specialist treatment improves outcomes.

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What is systemic inflammation?

Body-wide immune activation beyond local joints.

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Inflammatory markers used in RA

ESR and CRP.

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What are autoantibodies?

Antibodies directed against the body’s own tissues.

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What is a DMARD?

Disease-modifying antirheumatic drug.

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Purpose of DMARDs

Reduce inflammation and slow joint destruction.

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What are biologic DMARDs?

Targeted therapies against immune mediators.

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What are JAK inhibitors?

Targeted synthetic DMARDs affecting inflammatory signalling.

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Key cytokines in RA

TNF-alpha, IL-1 and IL-6.

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Nursing role in RA

Monitor symptoms, function, adherence, infection risk and medicine adverse effects.

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How does RA affect quality of life?

Pain, fatigue and disability can affect work, family and social participation.

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Difference between OA and RA pain timing

OA worsens with use, RA is often worse after rest/morning.

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Difference between OA and RA pathology

OA cartilage degeneration, RA autoimmune synovitis.