Med-Surg: Chapter 20: Connective Tissue Disorders: Rheumatoid Arthritis Flashcards

1
Q

Epidemiology

A
  • affects 1% of population
  • females 3x more likely to get it than males
  • genetics and environmental factors play a key role in development
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2
Q

Risk factors

A
  • first degree relatives with hx of RA
  • cigarette smoke
  • bacteria
  • viruses
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3
Q

Pathophysiology

A

-is a chronic, systemic, autoimmune inflammatory disease characterized by an inflammatory process that affects diarthrodial, or freely moving, joints, causing pain and swelling
-involved joints are distributed in a symmetrical fashion, meaning bilateral wrists, ankles, or knees
-primarily targets the synovial membrane
-an unknown antigen triggers an immune response, leading to synovial tissue damage
-the immune system fails to distinguish self from “non-self” and causes destruction to the synovium of joints
-inflammation of the synovium may lead to a dramatic increase in synovial fluid, impairing movement and causing pain
-the synovial membrane becomes thickened and promotes destruction of the joint
>in this process, antigens (substances that trigger an immune response in order to rid the body of that substance) activate monocytes and T lymphocytes; then immunoglobulin antibodies form immune complexes with antigens. Phagocytosis of the immune complexes generates an inflammatory reaction. Leukotrienes and prostaglandins are produced as a result of phagocytosis. Leukotrienes attract additional WBCs, and prostaglandins modify inflammation
-Collagenase, an enzyme that breaks down collagen, is also produced by leukotrienes and prostaglandins, leading to edema, proliferation of synovial membrane and pannus formation (a layer of vascular fibrous tissue), destruction of cartilage, and erosion of bone

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4
Q

Clinical Manifestations

A

-joint pain
-joint swelling
-erythema
-morning stiffness (longer than 30 minutes)
-fatigue
>onset is often insidious, with vague complaints of joint and muscle pain that evolves into joint pain with synovitis, inflammation of the synovial membrane, and can lead to joint destruction and deformity

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5
Q

Joint Deformities

A

if left untreated or inadequately treated, leads to irreversible joint damage and disability

  • swan-neck deformity caused by hyperextension of the proximal interphalangeal joints
  • boutonniere deformity caused by abnormal flexion of the proximal interphalangeal joints
  • ulnar deviation caused by the lateral deviation of the phalanges
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6
Q

Rheumatoid nodules

A

may be formed in subcutaneous tissue over bony prominences

-nodules mobile and nontender

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7
Q

Extra-articular (outside of the joint) clinical manifestations

A
  • Osteopenia (decreased bone density)
  • Muscle weakness
  • Episcleritis (red, painful inflammation of the episclera without discharge)
  • Scleritis (inflammation of the sclera, which produces deep ocular pain)
  • Pleuritis (inflammation of the lining surrounding the lungs)
  • Pleural effusion (excess fluid accumulation around the lungs)
  • Pericarditis (inflammation of the fibrous lining that surrounds the heart)
  • An enlarged spleen
  • Anemia
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8
Q

How do Patients typically present?

A
  • peripheral joint pain, which is usually symmetrical
  • complain of morning stiffness lasting greater than 30 minutes
  • symptoms persist 6 weeks or longer
  • synovitis; tenderness and synovitis are assessed by palpating each joint individually
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9
Q

Comparing Osteoarthritis and Rheumatoid Arthritis

A

> Osteoarthritis

  • morning stiffness less than 30 minutes
  • not immune mediated
  • joint involved: large weight-bearing joints such as hips and knees; PIPs, DIPs, CMC, First MTP, previously injured joints
  • symmetrical joint involvement: not typical
  • systemic organ involvement: no

> Rheumatoid Arthritis

  • morning stiffness more than 30 minutes
  • immune mediated
  • joint involved: MCPs, PIPs, MTPs, wrists, elbows, ankles, knees
  • symmetrical joint involvement: yes, very typical
  • systemic organ involvement: yes
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10
Q

Radiographs

A

conventional radiographs used to assess for bony erosions and joint-space narrowing

  • may be repeated during treatment to assess for disease progression and efficacy of pharmacological therapy
  • MRI may detect erosions not detected by conventional radiographs
  • Ultrasonography used to assess for synovitis and erosions not detectable by plain radiographs and good option for pts who refuse MRI b/c of cost or claustrophobia
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11
Q

Nonpharmacological Therapy

A
  • education about disease and management of disease
  • range-of-motion exercise to promote joint mobility, reduce stiffness, and improve muscle strength
  • aerobic exercise promotes cardiac health
  • physical and occupational therapies to teach appropriate exercises, how to protect joints, evaluate need for assistive devices, and proper use of devices
  • proper nutrition to maintain good health, prevent obesity, and decrease risk of heart disease
  • take rest periods to manage fatigue and joint pain
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12
Q

Pharmacological management

A

Goal= control the inflammation that leads to joint and tissue destruction, decreasing joint pain, synovitis, and stiffness, as well as maintaining joint function and preventing joint destruction
>analgesics, NSAIDS, and glucocorticoids:
-analgesics including acetaminophen and narcotic agents, provide only pain relief with no alteration in disease process
-anti-inflammatory medications provide pain relief and some reduction in inflammation but do not alter disease process
-glucocorticoids (prednisone) may be given orally IM< intra-articularly, or IV and can suppress inflammation and later the disease process but are not safe at high doses over long periods of time
>if disease does not respond to combination of analgesics, anti-inflammatory agents, and low dose prednisone, they are treated with disease-modifying antirheumatic drugs (DMARDs)

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13
Q

Disease-Modifying Antirheumatic Drugs (DMARDs)

A
  • methotrexate (Rheumatrex)
  • leflunomide (Arava)
  • hydroxychloroquine (Plaquenil)
  • sulfasalazine (Azulfidine)
  • Tofacitinib (Xeljanz)

> each alters the immune system in various ways, altering the inflammatory response to decrease inflammation and slow disease progression
may be used alone as monotherapy or in conjunction with one another
before use, inform provider of hx or exposure to active tuberculosis

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14
Q

Safety Alert: Methotrexate

A
  • must be monitored closely for hepatic toxicity while the dose is being escalated and periodically while on a maintenance dose
  • take folic acid daily to prevent side effects such as oral ulcers
  • avoid alcohol b/c of risk of hepatotoxicity
  • counsel female patients on proper birth control methods b/c of risk of teratogenicity, the capability of producing fetal malformation
  • patients with renal insufficiency require lower doses of methotrexate
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15
Q

Antirheumatic: Methotrexate (rheumatrex)

A

Mechanism of action:

  • unknown
  • thought to affect immune funciton
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16
Q

Antirheumatic: Sulfasalazine (Azulfidine)

A

systemically interferes with prostaglandin synthesis

17
Q

Antirheumatic: Hydroxychloroquine (Plaquenil)

A

impairs complement-dependent antigen-antibody reaction

18
Q

Antirheumatic: Leflunomide (Arava)

A

inhibits pyrimidine synthesis, resulting in antiproliferative and anti-inflammatory effects

19
Q

Antirheumatic: Tofacitinib (Xeljanz)

A

inhibits Janus Kinase; an inflammation mediator

20
Q

Surgical Interventions

A
  • joint replacement or fusion to help alleviate pain but may not actually improve function
  • may remove rheumatoid nodules, but may return over time
21
Q

Biological Therapy

A
  • Infliximab (Remicade)
  • Etanercept (Enbrel)
  • Adalimumab (Humira)
  • Rituximab (Rituxan)
  • Certolizumab (Cimzia)
  • Golimumab (Simponi)
  • Tocilizumab (Actemra)
  • Abatacept (Orencia)
22
Q

Complications of RA

A
  • decreased function of joints and permanent joint deformities, which may lead to permanent disability if the disease is not well controlled
  • extra-articular complications: increased risk of infection and developing cancer
23
Q

Nursing Management: Assessment and Analysis

A

clinical manifestations are r/t pain and decreased function of the affected joints

  • unsteady gait
  • bony enlargement or swelling of affected joints
  • warmth and redness of joints
  • painful range of motion of affected joints
  • increased incidence of infection
  • elevated serum creatinine secondary to NSAID use
  • elevated liver enzymes secondary to methotrexate or leflunomide
  • constipation secondary to decreased physical activity and/or use of narcotic analgesics
  • nausea or oral ulcers r/t methotrexate use
  • cough and/or SOB due to interstitial lung disease, which can be caused by RA or by methotrexate therapy
24
Q

Nursing Management: Assessment and Analysis

A

clinical manifestations are r/t pain and decreased function of the affected joints

  • unsteady gait
  • bony enlargement or swelling of affected joints
  • warmth and redness of joints
  • painful range of motion of affected joints
  • increased incidence of infection
  • elevated serum creatinine secondary to NSAID use
  • elevated liver enzymes secondary to methotrexate or leflunomide
  • constipation secondary to decreased physical activity and/or use of narcotic analgesics
  • nausea or oral ulcers r/t methotrexate use
  • cough and/or SOB due to interstitial lung disease, which can be caused by RA or by methotrexate therapy
  • self-care deficit
  • fatigue
25
Q

Nursing Assessments

A

> Joint pain and mobility
-indicators of treatment efficacy and disease progression

> Temperature
-increase in temperature = infection

> Laboratory Testing
C-reactive protein (CRP) and erythrocyte sedimentation rate ESR: elevated values = inflammation
Hemoglobin: may be less than normal in patients with active RA, but a decrease may = a GI bleed, caused by NSAID use
Serum Albumin: decreased value is correlated with increased disease severity b/c it is a negative acute-phase reactant and decreases in response to acute inflammation
Platelet Count: may be elevated in active disease b/c inflammation causes elevated platelet count
Liver and Renal Function: elevated levels may be due to medications used to treat RA

> Assess for peripheral effusion, pericarditis, pleuritic, scleritis, episcleritis, and osteopenia
-extra-articular clinical manifestations of RA may be present due to inflammatory changes outside the joints

26
Q

Nursing Actions

A

> Administer analgesics and anti-inflammatories as ordered
-analgesics and anti-inflammatories provide pain relief by reducing inflammation but do not alter the disease process

> Administer Glucocorticoids as ordered
-decrease pain by suppressing the inflammatory process and may alter the course of the disease

> Administer DMARD therapy
-very important in slowing the disease progression by modulating the immune system and decreasing the inflammatory response

> Administer Biologics
-been shown to slow or halt the progression of RA through inhibition of tumor necrosis factor (TNF) or interleukins (ILs)

27
Q

Teaching

A

> importance of adherence to treatment plan

> report s/s of infection
-b/c of treatment with anti-inflammatories and immunosuppressive therapy, must be aware of s/s

> immunosuppressive therapy should be discontinued while patients have an active infection
-immunosuppressive therapy puts patients at a higher risk for developing infections and complications from infections

> Assist with referral to an infectious disease specialist for patients with chronic or atypical infections
-patients with RA who are on immunosuppressive therapy are at risk for developing infections

> keep current with vaccinations
-risk for infections due to treatment but should not receive live vaccines

> refer to physical and occupational therapies as needed
-preserve joint function and improve quality of life

28
Q

Evaluating Care Outcomes

A

important assessments of the efficacy of pharmacological therapy are the amount of joint tenderness and synovitis the patient is experiencing and the duration of morning stiffness

  • have active patient involvement
  • importance of using anti rheumatoid medications properly and consistently
  • full efficacy cannot be achieved if the medication is not used consistently and that the medications can be dangerous if used more than directed
  • patient with well-controlled RA will have very few or no tender or swollen joints with minimal morning stiffness while experiencing little or no adverse effects from pharmacological therapy