Rheumatoid Arthritis Flashcards

1
Q

What is rheumatoid arthritis?

A

A chronic systemic autoimmune disease characterized by inflammation of connective tissue in the synovial joints that causes degeneration.

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2
Q

What is the pathophysiology of rheumatoid arthritis?

A

Begins when a genetically susceptible person has an immune response to an antigen. The antigen triggers formation of an abnormal immunoglobulin (IgG). Rheumatoid factor (RF) are the autoantibodies that respond to the abnormal IgG. Combine and lead to activation of inflammatory response, neutrophils attract to the site of inflammation and release enzymes that damage cartilage. CD4 cells cause WBCs to secrete cytokines that drive the inflammatory process.

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3
Q

What are the early clinical manifestations of RA?

A

General stiffness is the first sign. Morning stiffness, pain increased with motion. X-ray showing a narrowed joint space, articular cartilage destruction/erosion, and deformity.

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4
Q

What are the late clinical manifestations of RA?

A

Subluxation- muscle atrophy and tendon destruction. Poor alignment and fusion with advanced disease. Walking disability. Ulnar drift, Boutionniere, swan neck, and hallux vagus deformities.

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5
Q

What are other manifestations of RA?

A

Rheumatoid nodules- firm, nontender masses found on bony areas exposed to pressure (can occur anywhere). Scleral nodules, vocal cord nodules, nodules in heart and lungs with later disease. Sjogren’s disease- gums deteriorate, tooth loss, photosensitivity, eyes feel dry and gritty. Felty syndrome- affects the spleen; increased risk for infection due to low WBC count. Flexion contractures- structural changes that prevent movement of joints.

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6
Q

What are diagnostics used for RA?

A

History and physical (joint pain, swelling), lab tests (rheumatoid factor, antibodies to citrullinated peptide; anti-CCP). RF present in 80% of people, anti-CCP more specific than RF, 60-80% of patients, can be detected 5-10 years before onset of symptoms, level > 20 indicates possible RA. Elevated ESR and CRP. ANA titers indicator of autoimmune involvement. Synovial fluid analysis- MMP-3 increased (marker for progressive joint damage), increased WBCs. Tissue biopsy to confirm inflammatory changes. X-ray- soft tissue swelling and possible bone demineralization.

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7
Q

What are the diagnostic criteria for RA?

A

Patients should be tested for RA if they initially present with at least 1 joint with definite clinical synovitis and the synovitis is not explained by another disease. Score greater than or equal to 6 indicates presence of RA.

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8
Q

What is the first line of treatment for RA?

A

Disease-modifying anti rheumatic drugs (DMARDS)- slow progression of disease. Methotrexate is preferred for early treatment of patients. Sulfasalazine- increased risk of kidney stones, encourage adequate fluid intake. Hydroxychloroquine- need baseline eye exams for risk of vision loss. Leflunomide- blocks immune cell over production. Tofacitinib- treats moderate to severe RA, avoid live vaccines.

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9
Q

What is methotrexate?

A

Preferred DMARD for early treatment of RA. It is an antimetabolite which inhibits DNA, RNA, and protein synthesis. Lower risk of toxicity than other meds, side effects are rare but include bone marrow suppression and hepatotoxicity. This med is teratogenic, females within child bearing age need to use 2 methods of effective contraception during and THREE months are treatment has stopped. CBC and CMP should be frequently monitored, WBC count. Therapeutic effects seen within 4-6 weeks.

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10
Q

What are biologic response modifiers?

A

Used in patients with moderate to severe RA that are not responsive to DMARDS, but can also be used in adjunct. AKA immunotherapy. Tumor necrosis factor inhibitors- stop inflammation by targeting TNF. Ex. etanercept, infliximab, adalimumab, certolizumab, golimumab.

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11
Q

How are corticosteroids used in RA treatment?

A

Used to manage acute pain and inflammation. Given orally for limited time to decrease disease activity until DMARDS take effect, or given as intraarticular injections. Should not be used long-term, complication is osteoporosis. Monitor for weight gain.

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12
Q

What are non pharmacological therapies used in RA?

A

Rest, cold/ice, heat/hotpacks, exercise, gentle ROM exercise, joint preservation (use of joint protective devices).

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13
Q

What nutritional therapy is indicated in RA treatment?

A

Educate importance of balanced nutrition. Weight loss may result due to lack of appetite and limited mobility.

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14
Q

What kind of collaborative care is seen with RA?

A

PT- Assess patient’s current mobility, promote use of assistive devices, develop exercise plans and teach safety, coordinate with PT to medication before/after therapy, recommend and apply thermal therapies. OT- Assess impact of RA on ability to perform ADLs, teach use of assistive devices such as long handled grabbers, shoe horns, identify modifications needed. Social Worker- Assist with obtaining durable medical equipment, financial and psychosocial impact on patient.

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15
Q

What are nursing implementations for patients with RA?

A

Give drug therapy as ordered, teach about increased risk of infection with disease-modifying agents, develop program for rehabilitation, teach need for balance of rest and activity, aid with passive ROM of affected joints, assess quality of life and joint function, assess pain intensity and give analgesics, help patients with self care, educate on use of adaptive equipment.

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