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Chapter 64
Arthritis Connective
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Osteoarthritis
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2
Osteoarthritis (OA)

Slowly progressive noninflammatory disorder of the
diarthrodial joints

30 million Americans affected
• Numbers expected to increase as population ages

More common in women
• Especially hand OA and knee OA (after menopause)

Most men affected by 70 to 80 years, except for
traumatic arthritis
• Hip OA more common
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3
Case Study (1 of 7)
A.L. , a 47-year-old man, presents to a clinic with
pain in his right knee with activity. He has a
negative history for illnesses or trauma. He used to
play soccer regularly but has not played in 10
years. He claims the pain prevents him from
playing football with his teenage son.
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4
Case Study (2 of 7)
The health care provider suspects osteoarthritis
(OA). In preparation for teaching T.S. about this
disease process, you decide to quickly review its
etiology and pathophysiology.
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5
Case Study (3 of 7)

What causes OA?

Describe the pathophysiology of OA.
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6
Etiology and Pathophysiology (1 of
4)


Gradual loss of articular cartilage
Formation of osteophytes at joint margins


Not normal part of aging process
Cartilage destruction




Begins between ages 20 and 30
Most adults affected by age 40
Symptoms manifest after age 50 to 60
More than 50% over age 65 have x-ray evidence of
OA in at least 1 joint
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7
Etiology and Pathophysiology (2 of
4)



Secondary OA—caused by direct damage or joint
instability (see Table 64-1 in the textbook)
Idiopathic OA—event or condition may not be known;
genetics may contribute
Risk factors






Age
Decreased estrogen at menopause
Obesity
Anterior cruciate ligament injury
Frequent kneeling and stooping
Regular moderate exercise decreases risk
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8
Etiology and Pathophysiology (3 of
4)


Complex interaction of genetic, metabolic, and local
factors lead to the development of OA
Destruction of articular cartilage causes narrowing of
joint space (see slide 12)

Cartilage becomes:
• Dull, yellow, and granular
• Softer and less elastic
• Less able to resist wear with heavy use


Articular surfaces cracked and worn
Formation of osteophytes
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9
Etiology and Pathophysiology (4 of
4)
•
•
Inflammation and thickening of capsule and synovium
cause early stage pain and stiffness
Central cartilage is thinner; edges become thicker and
osteophytes are formed resulting in uneven weight
distribution; bones rub together leading to increasing
pain in later stages
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10
Pathologic Changes in OA
(Fig. 64-1)
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11
Case Study (4 of 7)

What clinical manifestations will you look for
when you assess A.L.?
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12
Manifestations: Joints (1 of 4)

Joint pain
 Primary symptom ranging from mild discomfort to
significant disability
 Pain worsens with joint use
• Early stages: rest relieves pain
• Later stages: pain with rest and trouble sleeping due to
increased joint pain
 Pain may worsen with lower barometric pressure
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13
Manifestations: Joints (2 of 4)

Pain contributes to disability and loss of function as
OA progresses



Pain may be referred to groin, buttock, or outside of
thigh or knee
Sitting down becomes difficult, as does getting up
from a chair when hips are lower than knees
OA in intervertebral (apophyseal) joints causes local
pain and stiffness
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14
Manifestations: Joints (3 of 4)

Joint stiffness occurs after periods of rest or
unchanged position

Early morning stiffness usually resolves within 30
minutes
• Distinguishes from rheumatoid arthritis

Overactivity leads to mild joint effusion, temporarily
increasing stiffness
 Crepitation (grating sensation)
 OA affects joints asymmetrically
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15
Manifestations: Joints (4 of 4)

Joints most affected by OA








Hips
Knees
Metatarsophalangeal
(MTP)
Cervical vertebrae
Lumbar vertebrae
Distal interphalangeal (DIP)
Proximal interphalangeal
(PIP)
Metacarpophalangeal
(MCP)
Fig. 64-2
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16
Manifestations: Deformity

Specific to joint involved
Heberden’s nodes: DIP (see slide 19)
 Bouchard’s nodes: PIP

• Appear red, swollen, and tender

Varus deformity (bowlegged): medial knee
 Valgus deformity (knock-kneed): lateral knee
 One leg shorter than the other: hip
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17
Heberden’s nodes
(Fig. 64-1D)
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18
Manifestations: Systemic


Fatigue, fever, and organ involvement are not
present
Distinguishes OA from other inflammatory
disorders, such as RA
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19
Case Study (5 of 7)
Upon examination of A.L.’s knee, no swelling is
noted, but crepitation is present.

What diagnostic studies would you expect the
health care provider to order for A.L.?
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20
Diagnostic Studies




Bone scan, CT scan, MRI
 Diagnosis of OA; show early joint changes
X-rays
 Detect joint space narrowing, increased bone density,
and osteophytes
No specific lab tests or biomarkers
 Baseline labs may be done before starting treatments
or for screening for related conditions
Synovial fluid analysis
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21
Case Study (6 of 7)
The health care provider orders an x-ray and MRI
of A.L.’s knee. The results show joint space
narrowing and osteophyte formation.
 What treatment would you expect the health
care provider to order?
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22
Interprofessional Care


See Table 64-2 in the textbook
No cure, care focuses on:

Managing pain and inflammation
 Preventing disability
 Maintaining and improving joint function


Nondrug interventions are the basis for OA management
Drug therapy supplements nondrug treatment
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23
Interprofessional Care
Rest and Joint Protection


Balance rest and activity
Rest during acute inflammation





Functional positioning with splints or braces
Avoid increased stiffness by limiting immobility to less
than 1 week.
Modify activities to decrease joint stress
Avoid prolonged standing, kneeling, or squatting
Assistive device as needed
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24
Interprofessional Care
Heat and Cold Applications
 May help reduce pain and stiffness
 Ice for acute inflammation
 Heat therapy for stiffness
•
Hot packs, whirlpool baths, ultrasound, and paraffin
wax baths
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25
Interprofessional Care
Nutritional Therapy and Exercise
 If overweight, weight-reduction critical
 Dietary changes as needed
 Exercise



Aerobic
Range of motion
Muscle strengthening
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26
Case Study (7 of 7)
The health care provider orders NSAIDs and rest
for A.L. during periods of acute inflammation but
not longer than 1 week. The patient asks you
about other treatment strategies.
 How would you respond?
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27
Complementary and
Alternative Therapies





See Complementary and Alternative Therapies box in
the textbook
Acupuncture
Massage
Tai Chi
Nutritional supplements


Glucosamine and chondroitin (not recommended by ACR
or AAOS)
Any supplements or therapies should be researched and
discussed with HCP
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28
Interprofessional Care
Drug Therapy (1 of 3)


Based on severity of patient’s symptoms
Mild to moderate joint pain




Acetaminophen
Topical agent (e.g., capsaicin cream)
OTC creams containing camphor, eucalyptus oil, and
menthol (e.g., BenGay, ArthriCare)
Topical salicylates (e.g., Aspercreme)
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29
Interprofessional Care
Drug Therapy (2 of 3)
•
Moderate to severe joint pain
•
Nonsteroidal antiinflammatory drug (NSAID); start low
dose, increase if needed





Ibuprofen 200 mg up to four times per day
Misoprostol to decrease GI side effects
Arthrotec (combination of misoprostol and NSAID diclofenac)
Diclofenac gel
Avoid both oral and topical NSAIDs together
•
COX-2 inhibitor celecoxib (Celebrex)
• Response to and cost of NSAIDs vary
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30
Interprofessional Care
Drug Therapy (3 of 3)

Intraarticular corticosteroid injections

4 or more injections without relief suggest need for
additional intervention
 Corticosteroids should not be given systemically

Hyaluronic acid injection—knee OA

Viscosupplementation
 No longer recommended

DMOADs—disease-modifying OA drugs

No drugs approved to modify OA progression

Strontium ranelate is being evaluated
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31
Interprofessional Care
Surgical Therapy
 Arthroscopic surgery



For patients with loss of function, unmanaged pain,
and decreased independence
Common for patients with knee OA
May provide no additional benefit over PT and
medical treatment
 Hip and knee replacement (see Chapter 62 in the
textbook)
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32
Nursing Assessment

Joint pain and stiffness




Type, location, severity, frequency, and duration;
aggravating or alleviating factors
Impact on ability to perform ADLs
Pain management practices
Assess affected joints (compare to unaffected)



Tenderness, swelling
Limitation of movement
Crepitation
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33
Nursing Diagnoses



Acute and chronic pain
Impaired mobility
Difficulty coping
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34
Planning

Overall goals


Maintain or improve joint function
Use joint protection measures
• See Patient and Caregiver Teaching: Table 64-4 in the
textbook


Achieve independence in self-care and maintain
optimal role function
Use drug and nondrug strategies for satisfactory pain
management
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35
Health Promotion (1 of 5)
 Community education

Alter modifiable risk factors
• Lose weight
• Reduce occupational/ recreational hazards
 Safety measures in athletic instruction and physical
fitness programs
 Prompt treatment of traumatic joint injuries
 See: Promoting Population Health section in the
textbook
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36
Acute Care (2 of 5)


Outpatient management with interprofessional team
Health assessment questionnaires to pinpoint areas
of decreased function



Complete at regular intervals
Individualized treatment goals
Hospitalized for joint surgery
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37
Acute Care (3 of 5)

Pain management and inflammation




Drugs
Nondrug strategies (massage, heat, cold, meditation,
yoga)
Splints
Physical therapy for exercise program


Tai Chi
Warm-up to prevent injury
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38
Acute Care (4 of 5)

Patient teaching





Nature and treatment of disease
Pain management
Body mechanics
Correct use of assistive devices
Joint protection and energy conservation
 See Table 64-4 in the textbook



Nutrition
Weight and stress management
Exercise
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39
Acute Care (5 of 5)

Patient support


Assure disease is localized; severe deforming arthritis
is not usual course of OA
Community resources: arthritis foundation
• www.arthritis.org
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40
Ambulatory Care (1 of 2)

Adjust home management goals

Include caregiver, family members, and
significant others
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41
Ambulatory Care (2 of 2)

Home and work environment modification



Eliminate scatter rugs; use railings and night lights
Wear well-fitting support shoes
Assistive devices
• Canes, walkers, elevated toilet seats,
grab bars

Sexual counseling
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42
Evaluation

Expected outcomes



Have adequate rest and activity
Achieve acceptable pain management
Maintain joint flexibility and muscle strength through
joint protection and therapeutic exercise
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43
Audience Response Question
(1 of 2)
The nurse determines that teaching about management of
osteoarthritis of the feet and hands has been effective
when the patient says:
a. “I will be careful to avoid crowds and people with
infections.”
b. “I can use heat to relieve the stiffness when I wake up in
the morning.”
c. “I should exercise my hands every day, especially if they
are painful and inflamed.”
d. “I should avoid the use of glucosamine as it does not
have any therapeutic value.”
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44
Audience Response Question
(2 of 2)
Answer: B
“I can use heat to relieve the stiffness when I wake
up in the morning.”
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45
Rheumatoid Arthritis
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46
Rheumatoid Arthritis (RA)
(1 of 3)

Chronic, systemic autoimmune disease;
inflammation of connective tissue in diarthrodial
(synovial) joints




Periods of remission and exacerbation
Extraarticular manifestations
Disabling form of arthritis causing loss of
independence and self-care
Mobility aids or joint reconstruction may be needed if
treatment inadequate
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47
Rheumatoid Arthritis (RA)
(2 of 3)





Affects all ethnic groups
Incidence increases with age, peaks between
ages 30 and 50
Estimated 1.5 million Americans
Three times as many women as men
See the Cultural and Ethnic Health Disparities
section in the textbook
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48
Case Study (1 of 11)
T.S. is a 40-year-old woman who presents to the
clinic with fatigue, morning stiffness, and painful
swelling of her fingers. The health care provider
suspects rheumatoid arthritis (RA).
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49
Case Study (2 of 11)

In preparation for teaching T.S. about this
disease process, you decide to quickly review its
etiology and pathophysiology.
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50
Case Study (3 of 11)

What causes RA?

Describe the pathophysiology of RA.
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51
Etiology and Pathophysiology
(1 of 4)

Autoimmune etiology



Combination of genetics and environmental triggers
Antigen triggers formation of abnormal
immunoglobulin G (IgG)
Autoantibodies develop against the abnormal IgG

Rheumatoid factor (RF)
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52
Etiology and Pathophysiology
(2 of 4)


Rheumatoid factor combines with IgG to form
immune complexes that deposit on synovial
membranes or cartilage in joints; this leads to
activation of complement and inflammatory
response
Neutrophils release proteolytic enzymes that
damage cartilage and thicken synovial lining
(see slide 56)
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53
Etiology and Pathophysiology
(3 of 4)

T helper cells (CD4) activated, stimulating
monocytes, macrophages, and synovial fibroblasts
to secrete proinflammatory cytokines



Interleukin-1 (IL-1)
Interleukin-6 (IL-6)
Tumor necrosis factor (TNF)
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54
Rheumatoid Arthritis (3 of 3)
Fig. 64-3
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55
Etiology and Pathophysiology
(4 of 4)

Genetic link

Genetic predisposition important in RA development
• Role of human leukocyte antigens (HLA)
• HLA-DR4 and HLA-DR1 antigens

Smoking increases risk in patients genetically
predisposed and may interfere with treatment
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56
Case Study (4 of 11)

What other clinical manifestations of RA will you
assess for in T.S.?
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57
Manifestations: Joints (1 of 4)



Onset typically subtle
Fatigue, anorexia, weight loss, generalized stiffness
that becomes localized stiffness with progression
May report history of precipitating stressful event


Infection, stress, exertion, childbirth, surgery,
emotional upset
No direct correlation found in research
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58
Manifestations: Joints (2 of 4)

Specific joint involvement




Pain, stiffness, limited motion, and signs of
inflammation
Symptoms occur symmetrically
Often affects small joints (PIP, MCP, and MTP)
Larger joints and cervical spine may be involved

See Table 64-5 in the textbook for Comparison of RA
and OA
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59
Manifestations: Joints (3 of 4)






Joint stiffness after inactivity
Morning stiffness 60 minutes to several hours or
longer
MCP and PIP joints typically swollen
Fingers spindle shaped
Joints tender, painful, warm to touch
Pain increases with motion, intensity varies
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60
Manifestations: Joints (4 of 4)





Tenosynovitis affects wrists, CTS symptoms
With progression, inflammation and fibrosis may
cause deformity and disability
Subluxation—muscle atrophy and tendon
destruction
Walking disability (see slide 56)
Deformities in the hands

Ulnar drift, swan neck, and boutonnière’s deformity
(see slide 63)
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61
Typical Deformities of Rheumatoid
Arthritis (Fig. 64-4)
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62
Extraarticular Manifestations (1 of
2)


See slide 66
Affects all body systems

Rheumatoid nodules
• Firm, nontender masses found on bony areas exposed
to pressure
• Cataracts and vision loss
• Nodular myositis
• Pleurisy, pleural effusion, pericarditis, pericardial
effusion, and cardiomyopathy
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63
Extraarticular Manifestations (2 of
2)

Sjögren’s syndrome
• Dry, gritty eyes and photosensitivity

Felty syndrome
• Enlarged spleen and low WBCs result in increased risk
of infection and lymphoma

Flexion contractures
• Decreased self-care

Depression
• Pain and disability
• Increased C-reactive protein levels
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64
Extraarticular Manifestations of
Rheumatoid Arthritis (Fig. 64-5)
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65
Diagnostic Studies (1 of 2)


History and physical findings
Criteria for diagnosis (see Table 64-6 in the
textbook)




Joint involvement
Serology
Acute phase reactants
Duration of symptoms
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66
Case Study (5 of 11)
The results of T.S.’s hand x-rays show no
significant abnormality.

In what stage would T.S.’s RA be classified?
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67
Stages of Rheumatoid Arthritis (1 of
2)



See Table 64-7 in the textbook.
Progression
Stage I

Synovitis
 X-ray: soft tissue swelling, possible osteoporosis, no joint
destruction

Stage II

Increased joint inflammation
 Gradual destruction in joint cartilage
 Narrowing joint space from loss of cartilage
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68
Stages of Rheumatoid Arthritis (2 of
2)

Stage III



Formation of synovial pannus
X-ray: extensive cartilage loss, erosion at joint
margins, possible deformity
Stage IV



Inflammatory process subsides
Loss of joint function
Formation of subcutaneous nodules
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69
Case Study (6 of 11)

What diagnostic testing would you expect the
health care provider to order for T.S.?
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70
Diagnostic Studies (2 of 2)

Lab tests (see Table 64-8 in the textbook)







CBC
ESR: active inflammation
CRP: active inflammation
RF (positive in 80% of adults)
Anti-CCP: antibody specific to RA
ANA: autoimmune reaction
Other:



Bone scans: early joint changes
X-rays: progression
Synovial fluid analysis: cloudy, straw-colored fluid with fibrin
flecks and MMP-3
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71
Case Study (7 of 11)
T.S.’s lab results indicate positive RF and ANA.
Her CRP and ESR are also elevated. The health
care provider tells T.S. she has rheumatoid
arthritis.
 What medication(s) would you expect the health
care provider to prescribe for T.S.?
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72
Interprofessional Care


See Table 64-8 in the textbook
Individualized treatment plan considers:







Disease activity
Joint function
Age
Sex
Family and social roles
Response to previous treatment
Aggressive early treatment improves prognosis
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73
Drug Therapy



See Tables 64-3 and 64-9 in the textbook
Drugs are cornerstone of treatment; irreversible
changes can occur in the first year; HCPs prescribe:
Disease-modifying antirheumatic drugs (DMARDs )
• Slow disease progression and decrease risk of
joint deformity and erosion
• Drug chosen based on disease activity, functional
level, and lifestyle considerations
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74
Drug Therapy: DMARDs (1 of 3)

Methotrexate





Early treatment
Lower toxicity
Side effects (rare): bone marrow suppression and
hepatotoxicity
Need to monitor CBC and blood chemistry
Therapeutic effects in 4 to 6 weeks; may be given
alone or with biologic response modifiers
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75
Drug Therapy: DMARDs (2 of 3)

Sulfasalazine (Azulfidine) and hydroxychloroquine
(Plaquenil)




Used for mild to moderate disease
Drink fluids
Wear sunscreen
Eye exam: baseline, then every 6 to 12 months
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76
Drug Therapy: DMARDs (3 of 3)

Leflunomide (Arava)



Blocks immune cell overproduction
Not used during pregnancy; teratogenic
Tofacitinib (Xeljanz)



JAK (Janus kinase) inhibitor: interferes with enzymes
that cause joint inflammation
Moderate to severe active disease
No live vaccines
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77
Drug Therapy: Biologic Response
Modifiers (BRMs) (1 of 4)

Also called biologics or immunotherapy




Slow progression
Classified based on mechanism of action (see Table
64-9 in the textbook)
Used to treat moderate to severe disease not
responsive to DMARDs
Used alone or in combination with DMARDs
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78
Drug Therapy: BRMs (2 of 4)

Tumor necrosis factor (TNF) inhibitors bind with
TNF, inhibiting inflammation

Etanercept (Enbrel): subcutaneous
• Biologically engineered copy of TNF receptor


Infliximab (Remicade): IV infusion
Adalimumab (Humira): subcutaneous
• Monoclonal antibodies

Certolizumab (Cimzia)
 Golimumab (Simponi)
• TNF inhibitors
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79
Drug Therapy: BRMs (3 of 4)

Tumor necrosis factor (TNF) inhibitors




TB test and chest x-ray before start of therapy
Monitor for infection
Avoid live vaccinations
Report bruising, bleeding, persistent fever, and other
signs of infection
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80
Drug Therapy: BRMs (4 of 4)

Anakinra (Kineret): given SQ



Tocilizumab (Actemra)


Blocks IL-6, a proinflammatory cytokine
Abatacept (Orencia): given IV


IL-1 receptor antagonist (IL-1Ra)
Reduces pain and swelling
Blocks T-cell activation
Rituximab (Rituxan): given IV


Monoclonal antibody
Targets B cells
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81
Other Drug Therapy (1 of 2)

Not commonly used



Immunosuppressants (azathioprine [Imuran])
Penicillamine (Cuprimine)
Gold preparations (auranofin [Ridaura])
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82
Other Drug Therapy (2 of 2)

Corticosteroid therapy


Intraarticular injections
Low-dose oral for limited time
• Complications: osteoporosis and avascular necrosis

NSAIDs and salicylates



Treat pain and inflammation
May take 2 to 3 weeks for full effectiveness
Celecoxib (Celebrex): COX-2 inhibitor
• Non-aspirin NSAIDs increase risk of blood clots, heart
attack, and stroke
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83
Nutritional Therapy




Balanced nutrition important
Pain, fatigue, and depression lead to decreased
appetite
Lower endurance and mobility cause inability to
shop for and prepare food resulting in weight
loss; work with OT for plan
Corticosteroid therapy, resulting in weight gain
Copyright © 2020 by Elsevier, Inc. All rights reserved.
84
Surgical Therapy




Relieve severe pain
Improve function
Synovectomy
Total joint replacement (arthroplasty)
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85
Nursing Assessment (1 of 6)


See Table 64-10 in the textbook
Subjective data
 Past health history: recent infections, presence of
precipitating factors, pattern of remissions and
exacerbations
 Medications: aspirin, NSAIDs, corticosteroids,
DMARDs, BRMs
 Surgery or other treatments: any joint surgery
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86
Nursing Assessment (2 of 6)

Subjective data

Functional health patterns
• Health perception–health management: family history,
malaise, ability to participate in therapeutic regimen,
impact on functional ability
• Nutritional–metabolic: anorexia, weight loss, dry
mucous membranes of mouth, and pharynx
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87
Nursing Assessment (3 of 6)

Subjective data
• Activity–exercise: stiffness and joint swelling,
muscle weakness, difficulty walking, fatigue
• Cognitive–perceptual: paresthesia of hands and
feet, loss of sensation, symmetric joint pain and
aching that increase with motion or stress on joint
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88
Nursing Assessment (4 of 6)

Objective data



General: lymphadenopathy, fever
Integumentary: scleritis, subcutaneous nodules, skin
ulcers, shiny, taut skin over joints, peripheral edema
Cardiovascular: Raynaud’s phenomenon, distant
heart sounds, murmurs, dysrhythmias
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89
Nursing Assessment (5 of 6)

Objective data


Respiratory: bronchiectasis, pleural effusion,
tuberculosis, interstitial lung disease
Gastrointestinal: splenomegaly (Felty syndrome)
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90
Nursing Assessment (6 of 6)

Objective data

Musculoskeletal: symmetric joint involvement,
swelling, erythema, heat, tenderness, deformities,
joint enlargement, limitation of movement, muscle
contractures, muscle atrophy
 Possible diagnostic findings: positive RF, ANA, antiCCP, elevated ESR, anemia, elevated WBCs in
synovial fluid, x-ray evidence of joint changes
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91
Nursing Diagnoses




Impaired mobility
Chronic pain
Disturbed body image
See eNursing Care plan 64-1 on the Evolve
website
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92
Planning

Overall goals





Satisfactory pain management
Minimal loss of functional ability
Participate in therapeutic regimen
Maintain positive self-image
Perform self-care
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93
Health Promotion



Prevention not possible
Early treatment to prevent further joint damage
Community education programs


Symptom recognition to promote early diagnosis and
treatment
Resource: The Arthritis Foundation
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94
Acute Care



Most care is outpatient
Hospitalized for systemic complications or surgery
Work with HCP, PT, OT, and social worker

See Nursing Management: Caring for the Patient with
Rheumatoid Arthritis box in the textbook
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95
Case Study (8 of 11)

What type of nondrug interventions could you
include in teaching for T.S. to help with her joint
pain?
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96
Case Study (9 of 11)

What interventions can you teach T.S. to help
manage her fatigue?
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97
Ambulatory Care


Drug therapy
Nondrug therapy







Balance of rest and activity
Heat and cold application
Relaxation techniques
Joint protection (see Tables 64-4 and 64-11 in the
textbook)
Biofeedback
TENS
Hypnosis
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98
Ambulatory Care
Rest (1 of 2)

Alternate rest periods with activity


Amount of rest varies



Helps relieve pain and fatigue
Avoid total bed rest
8 to 10 hours of sleep plus daytime rest
Modify activities to avoid overexertion
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99
Ambulatory Care
Rest (2 of 2)





Firm mattress or bed board
Encourage positions of extension
Avoid flexion positions
No pillows under knees
Small, flat pillow under head and shoulders
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100
Case Study (10 of 11)

What will you teach T.S. to help her protect her
joints from further stress?
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101
Ambulatory Care
Joint Protection


Modify tasks for less stress on joints (see Table 64-11 in
the textbook)
Energy conservation






Work simplification techniques
Pacing and organizing
Use of carts
Joint protective devices
Delegation
Occupational therapy

Assistive devices
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102
Case Study (11 of 11)
T.S. asks you whether she should use ice or heat
on her painful joints.

How will you respond?
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103
Ambulatory Care: Cold and Heat
Therapy and Exercise (1 of 4)


Relieve pain, stiffness, and muscle spasm
Cold



Especially beneficial during periods of disease activity
Application should not exceed 10 to 15 minutes at
one time
Bags of frozen vegetables, ice
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104
Ambulatory Care: Cold and Heat
Therapy and Exercise (2 of 4)

Moist heat



Relieve chronic stiffness
Should not exceed 20 minutes at a time
Heating pads, moist hot packs, paraffin baths, warm
baths, or showers
• Do not use with topical heat-producing cream

Be alert for burn potential
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105
Ambulatory Care: Cold and Heat
Therapy and Exercise (3 of 4)

Individualized exercise plan to




Improve flexibility and strength
Increase overall endurance
Encourage program participation and reinforce
correct performance
Need both recreational and therapeutic exercise

Avoid overly aggressive exercise
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106
Ambulatory Care: Cold and Heat
Therapy and Exercise (4 of 4)



Gentle ROM exercises done daily to keep joints
functional
Aquatic exercises in warm water beneficial
Limit to one or two repetitions during acute
inflammation
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107
Patient and Caregiver Education

Thorough program of education and drug therapy



Disease process
Home management
Drugs, administration/timing, action, side effects, lab
monitoring
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108
Psychologic Support (1 of 3)

Effective self-management and adherence
requires an understanding of:
 RA
 Nature
and course of disease
 Goals of therapy

Consider value system and perception of
disease
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109
Psychologic Support (2 of 3)

Patient challenges:







Limited function and fatigue
Loss of self-esteem
Altered body image
Fear of disability or deformity
Alterations in sexuality
Unproven or even dangerous remedies
Recognize fears and concerns
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110
Psychologic Support (3 of 3)





Evaluate family support system
Financial planning
Consider community resources
Self-help groups are helpful for some patients
Strategies to decrease depression
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111
Gerontologic Considerations (1 of
2)


Increased prevalence with older adults
Other areas of concern:
•
•
•
•
May also have OA
Interpretation of lab values more difficult
Polypharmacy can lead to joint pain
Musculoskeletal pain and weakness may be related to
depression and inactivity
• Other diseases may develop in milder forms, such as
SLE
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112
Gerontologic Considerations (2 of
2)


Older patients may be more sensitive to therapeutic
and toxic drug effects
Polypharmacy can cause increased interactions



Need simple plan to improve adherence
Osteopenia with corticosteroids may increase risk of
pathologic fractures
Needs support system
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113
Audience Response Question
(1 of 2)
Etanercept (Enbrel) is prescribed for a patient with
stage II rheumatoid arthritis. The nurse determines
that the medication is effective if what is observed?
a. Decreased lymphocyte count
b. Absence of Rh factor in the blood
c. Decreased C-reactive protein (CRP)
d. Increased serum immunoglobulin G
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114
Audience Response Question
(2 of 2)
Answer: C
Decreased C-reactive protein (CRP)
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115
Gout
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116
Gout (1 of 2)



Type of arthritis characterized by hyperuricemia
and deposition of uric acid crystals in one or
more joints
Sodium urate crystals may be in articular,
periarticular, and subcutaneous tissues
Painful flares for days to weeks, then long
asymptomatic periods
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117
Gout (2 of 2)

Incidence in United States greater than 8 million




Blacks more than whites
Men three times more than women
Develops in men age 30 to 50
Women rarely have gout before menopause
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118
Gout: Etiology and
Pathophysiology (1 of 2)

Uric acid is the end product of purine metabolism;
excreted by kidneys



Gout occurs if kidneys can’t excrete enough or if too
much is being made
Primary hyperuricemia: genetic
Secondary hyperuricemia: increased production,
decreased excretion, or drugs that inhibit uric acid
excretion; organ transplant recipients getting
immunosuppressants also at risk
Copyright © 2020 by Elsevier, Inc. All rights reserved.
119
Gout: Etiology and
Pathophysiology (2 of 2)

Caused by interaction of factors





Metabolic syndrome
Increased intake of high purine foods
Prolonged fasting
Excessive alcohol
Two processes must occur


Crystallization
Inflammation
• Phagocytosis causes increased inflammation and
tissue damage
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120
Clinical Manifestations (1 of 4)

One or more joints (usually less than 4)





Most common is the great toe (podagral)
Other: wrists, knees, ankles, midfoot, olecranon
bursae
Dusky or cyanotic
Very tender
Triggers: trauma, surgery, alcohol, or systemic
infection
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121
Clinical Manifestations (2 of 4)

Symptom onset at night




Sudden swelling and severe pain
Sensitive to light touch
Low-grade fever
Duration of 2 to 10 days with or without treatment
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122
Clinical Manifestations (3 of 4)

Chronic Gout


Multiple joint involvement
Tophi are visible deposits of crystals in subcutaneous
tissues, synovial membranes, tendons, and soft
tissues (see slide 125); occur years after onset
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123
Tophi of Chronic Gout
(Fig. 64-6)
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124
Clinical Manifestations (4 of 4)

Severity of gout is variable


It may involve infrequent, mild attacks or multiple
severe episodes (up to 12 per year) with slow,
progressive disability
High serum uric acid causes increase in episodes and
tophi
• Chronic inflammation leads to joint deformity, cartilage
destruction, secondary OA
• Large crystal deposits may pierce skin, draining
sinuses and causing infection
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125
Complications

Excessive uric acid excretion leads to kidney or
urinary tract stones

Pyelonephritis contributes to kidney disease
Copyright © 2020 by Elsevier, Inc. All rights reserved.
126
Diagnostic Studies





Serum uric acid higher than 6 mg/dL
24-hour urine for uric acid
Synovial fluid aspiration
Clinical symptoms
X-ray of affected joint
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127
Interprofessional and Nursing
Management (1 of 4)

Goals (see Table 64-13 in the textbook):



End acute attack
Control hyperuricemia and gout with patient education
and adherence
Drug therapy

Oral colchicine: antiiflammatory
• Pain relief in 12 hours: aids in diagnosis



NSAIDs: analgesia
Corticosteroids: oral or intraarticular
ACTH
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128
Interprofessional and Nursing
Management (2 of 4)

Drug therapy

Prevention
• Xanthine oxidase inhibitor: decreases uric acid
production; for example, allopurinol (Zyloprim or
Aloprim) or febuxostat (Uloric)
• Probenecid—uricosuric: increase urinary excretion of
uric acid; must avoid aspirin
• Lesinurad (Zurampic): uricosuric (new)
• Duzallo—combination lesinurad and allopurinol
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129
Interprofessional and Nursing
Management (3 of 4)

Drug therapy

Uricosurics
• Can cause renal impairment; take with food and water;
recommend 2 L/day

Alternates:
• Pegloticase (Krystexxa)

Metabolizes uric acid to harmless chemical
• Losartan (Cozaar): older adult with gout and HTN
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130
Interprofessional and Nursing
Management: Gout (4 of 4)


Monitor serum uric acid regularly
Dietary restrictions
 Limit
alcohol and food high in purine (see Table
45-12 in the textbook); teach about other factors
 Adequate urine volume
 Weight reduction

Nursing interventions
 Supportive
care of inflamed joint
 Assess motion limitations and pain
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131
Lyme Disease
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132
Lyme Disease

Borrelia burgdorferi infection transmitted by deer tick
bite

Most common vector-borne disease in United States; 7.9
cases per 100,000 people
 No person-person transmission
 Summer is time of peak transmission
 Three areas in United States
• Northeast: Maryland to Massachusetts
• Midwest: Wisconsin and Minnesota
• Northwest coast: California and Oregon

Reinfection common
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133
Manifestations (1 of 2)

Characteristic: erythema migrans (EM)

Bull’s eye rash (see slide 136)—occurs in 80%
• Appears within 1 month of exposure
• May occur elsewhere on body with disease progression
• Central red macule or papule expanding to outer red ring up
to 12 in
• Warm to touch; not itchy or painful
• Occurs with acute flu-like symptoms:


Low-grade fever, headache, neck stiffness, fatigue, loss of
appetite, migratory joint, and muscle pain
Resolve over weeks to months, even without treatment
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134
Erythema Migrans (EM)
(Fig. 64-7)
Copyright © 2020 by Elsevier, Inc. All rights reserved.
135
Manifestations (2 of 2)

Without treatment can spread to heart, joints, and
CNS

Arthritis: second most common symptom
• 60% get chronic arthritic pain; knee


Cardiac: heart block and pericarditis
Neurologic: Bell’s palsy
• Other: short-term memory loss, cognitive impairment,
shooting pains, numbness, and tingling in feet
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136
Diagnosis of Lyme Disease


Based on manifestations (e.g., EM) and history of
exposure
CDC recommends two step testing




1. Enzyme immunoassay (EIA)
2. Western blot test
Both positive confirms Lyme disease
CNS symptoms: CSF examination
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137
Interprofessional Care

Oral antibiotics
• Doxycycline, cefuroxime, and amoxicillin: early
treatment and prevention of progression


Preferred: 10 to 21 days doxycycline
Also treats co-infection of human granulocytic
anaplasmosis

Neurologic and cardiac complications: treat with IV
ceftriaxone or penicillin
 Some need extended antibiotic treatment
 Prevention: reduce exposure (see Table 64-14 in the
textbook)
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138
Septic Arthritis
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139
Septic Arthritis (1 of 3)


Infectious or bacterial arthritis
Microorganism invades joint cavity
 Hematogenous
spread, trauma or surgical
incision
 Most common: Staphylococcus aureus

Risk factors:
 Diseases
with decreased host resistance
 Corticosteroid or immunosuppressant therapy
 Debilitating chronic illness
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140
Septic Arthritis (2 of 3)


Most affected joints: knee and hip
Symptoms: severe pain, redness, and swelling;
fever, shaking chills


Hip: avascular necrosis
Diagnosis:




Arthrocentesis (joint aspiration)
Synovial fluid culture
WBC count
Blood cultures
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141
Septic Arthritis (3 of 3)

Treatment:
 Aspiration
or surgical drainage—emergent to
avoid irreversible joint damage
 Broad-spectrum antibiotics until culture
identification; IV transitioned to oral; 4 to 6 weeks




Assess and monitor joint inflammation
Pain management
Gentle ROM
Patient education about treatment
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142
Spondyloarthropathies
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143
Spondyloarthropathies (1 of 2)




Group of multisystem inflammatory disorders
affecting the spine, peripheral joints and
periarticular structures.
Includes: ankylosing spondylitis, psoriatic
arthritis, and reactive arthritis
Seronegative arthroplasties are RF negative
Genetic and environmental factors
 HLA-B27
associated with these diseases
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144
Spondyloarthropathies (2 of 2)

Difficult to distinguish in early disease

Laboratory and clinical characteristics include:
 Absence
of serum antibodies
 Peripheral joint involvement
 Low back pain (sacroiliitis)
 Redness of eyes (uveitis)
 Intestinal inflammation
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145
Ankylosing Spondylitis

Chronic inflammatory disease that primarily affects
axial skeleton

Sacroiliac joints, intervertebral disc spaces, and
costovertebral articulations
 Onset: 30’s or adolescence
 Men three times greater than women
 Women have milder course; undetected
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146
Ankylosing Spondylitis:
Etiology and Pathophysiology

Precise cause unknown

HLA-B27 antigen is present in 90% of whites
• Also see in Asians and Hispanics
• See Genetics in Clinical Practice box in the textbook

Manifestations

Inflammation of joints and adjacent tissue leads to
granulation tissue formation and dense fibrous scars that
can cause joint fusion
 Inflammation affects: eyes, heart, kidneys, lungs, and PNS
Copyright © 2020 by Elsevier, Inc. All rights reserved.
147
Clinical Manifestations





Inflammatory spine pain is first sign
Low back pain, stiffness, and limitation of
motion that is worse in morning and night;
improves with mild activity
Uveitis may present before arthritic symptoms
Chest pain and sternal/costal tenderness
Postural abnormalities and deformities (see slide
151)
148
Complications


Aortic insufficiency and pulmonary fibrosis
Cauda equina syndrome
 Lower
extremity weakness and bladder
dysfunction

Osteoporosis raises risk of spinal fractures
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149
Advanced ankylosing spondylitis
Fig. 64-8
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150
Ankylosing Spondylitis:
Diagnostic Studies

X-rays
 Late:
“bamboo spine” calcifications
(syndesmophytes)





MRI
CT scan
Elevated ESR
Mild anemia
HLA-B27 antigen
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151
Interprofessional Care


Cannot prevent; family history important
Maintain skeletal mobility

Decrease pain and inflammation
• Heat; hydrotherapy
• NSAIDs and salicylates; DMARDs; corticosteroid injections
• BRM and anti-TNF


Exercise plan
Surgery: spinal osteotomy and total joint replacement
are most common procedures
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152
Nursing Management

Patient education


Disease and principles of therapy
Home management
• Exercise, posture
• Heat
• Drugs






Assess chest expansion
Smoking cessation
Physical therapy focused on ROM & exercise
Avoid excessive exertion
Proper posture and positioning
Family counseling and vocation rehabilitation
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153
Psoriatic Arthritis (PsA) (1 of 4)

Progressive inflammatory disorder

Affects 30% of people with psoriasis
• Common, benign, inflammatory skin disorder with red,
irritated, and scaly patches
• Linked to HLA antigens; believed to have genetic,
immune, and environmental factors
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154
Psoriatic Arthritis (PsA) (2 of 4)

Distal arthritis: ends of fingers and toes
• Pitting and color changes to nails




Asymmetric arthritis: different joints on each side of
the body
Symmetric psoriatic arthritis: joints on both sides of
the body at the same time
Psoriatic spondylitis: pain and stiffness in spine and
neck
Arthritis mutilans: complete destruction of small joints;
most severe
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155
Psoriatic Arthritis (PsA) (3 of 4)

Diagnostic studies

X-ray
• DIP joints, “pencil in cup” deformity



Elevated ESR
Mild anemia
Elevated serum uric acid
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156
Psoriatic Arthritis (PsA) (4 of 4)

Treatments




Splinting
Joint protection
Physical therapy
NSAIDs, DMARDs, BRMs
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157
Reactive Arthritis (Reiter’s
Syndrome)

Symptom complex of urethritis, conjunctivitis,
and mucocutaneous lesions
 Cause
unknown; believed to be triggered by
specific GU or GI infection
• Chlamydia trachomatis, Shigella, Salmonella,
Campylobacter, or Yersinia or other
 HLA-B27
positive are at increased risk when
exposed to pathogens; genetic predisposition
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158
Manifestations of Reactive Arthritis

Urethritis develops 1 to 2 weeks after sexual
contact or GI infection followed by low-grade
fever, conjunctivitis, and arthritis




Women also get cervicitis
Asymmetric; involves toes and large joints of
lower extremities; low back pain
Skin and mucous membrane lesions
Achilles tendonitis or plantar fasciitis
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159
Interprofessional Care

Diagnostic studies


Elevated ESR
Treatment




Doxycycline for patient and sexual partners
Ophthalmic corticosteroids for uveitis
NSAIDs and DMARDs for joint symptoms
PT
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160
Systemic Lupus Erythematosus
(SLE)
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161
Systemic Lupus Erythematosus (1
of 3)


Multisystem inflammatory autoimmune disease
Complex multifactorial disorder




Genetic
Hormonal
Environmental
Immunologic
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162
Systemic Lupus Erythematosus (2
of 3)

Affects

Skin
 Joints
 Serous membranes
• Pleura
• Pericardium

Renal system
 Hematologic system
 Neurologic system
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163
Systemic Lupus Erythematosus (3
of 3)

Unpredictable course with alternating periods of
remission and worsening disease

In United States, 1.5 million have SLE
 More common in blacks, Asian Americans, Hispanics,
and Native Americans than in Whites
 90% are women ages 15 to 45 years
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164
Etiology and Pathophysiology (1 of
2)

Unknown cause of abnormal immune response;
type III hypersensitivity response

Most probable causes
• Genetic influence: high prevalence among family
members; HLA complex
• Hormones: menses, oral contraceptives, pregnancy
• Environmental factors: sun, UV light, stress, chemicals,
toxins; infectious agents
• Drugs: procainamide, hydralazine, quinidine, and
others
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165
Etiology and Pathophysiology (2 of
2)

Autoantibodies made against:
• Single- and double-stranded DNA, erythrocytes,
coagulation proteins, lymphocytes, platelets, and other
proteins


Autoimmune reactions (antinuclear antibodies)
directed against cell nucleus, especially DNA
Circulating immune complexes deposited in
basement capillary membranes of kidneys, heart,
skin, brain, and joints
• Overaggressive autoimmune responses are related to
activation of B and T cells
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166
Clinical Manifestations and
Complications (1 of 8)

Severity of SLE is extremely variable



Ranges from a relatively mild disorder to rapidly
progressive disease affecting many body systems
(see slide 169)
Most commonly affects skin, muscles, lining of lungs,
heart, nervous tissue, and kidneys
General: fever, weight loss, joint pain, and excessive
fatigue precede worsening disease activity
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167
Multisystem Involvement of SLE
(Fig. 64-9)
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168
Clinical Manifestations and
Complications (2 of 8)

Dermatologic problems

Vascular skin lesions
• Most commonly in sun-exposed areas

Butterfly rash (see slide 171)
• Occurs in 55% to 85% of cases





Chronic cutaneous lupus
Subacute cutaneous lupus (SCLE)
Oral/nasopharyngeal ulcers
Alopecia
Dry, itchy, atrophied scalp
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169
Butterfly Rash of SLE
(Fig. 64-10)
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170
Clinical Manifestations and
Complications (3 of 8)

Musculoskeletal problems

Polyarthralgia with morning stiffness
• Diffuse swelling

Arthritis
• Swan neck deformity in fingers (see slide 173)
• Ulnar deviation
• Subluxation with hyperlaxity of joints

Increased risk of bone loss and fracture
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171
Swan Neck Deformity
(Fig. 64-4D)
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172
Clinical Manifestations and
Complications (4 of 8)

Cardiopulmonary problems




Tachypnea
Cough
Pleurisy
Dysrhythmias
• Fibrosis of SA and AV nodes


Pericarditis, myocarditis, and endocarditis
Antiphospholipid syndrome
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173
Clinical Manifestations and
Complications (5 of 8)

Renal problems

Mild proteinuria to rapidly progressive
glomerulonephritis
 Scarring, permanent damage can lead to end-stage
renal disease
 Goal is slow progression of nephropathy and
preserve renal function
 Effective treatments are available
• Corticosteroids, cytotoxic agents, immunosuppressive
agents
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174
Clinical Manifestations and
Complications (6 of 8)

Nervous system problems



Generalized/focal onset seizures
Peripheral neuropathy
Cognitive dysfunction
• Disordered thinking
• Disorientation
• Memory deficits

Psychiatric disorders
 Stroke, aseptic meningitis
 Headache
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175
Clinical Manifestations and
Complications (7 of 8)

Hematologic problems

Formation of antibodies against
blood cells
•
•
•
•
Anemia
Leukopenia
Thrombocytopenia
Coagulation disorders

Warfarin
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176
Clinical Manifestations and
Complications (8 of 8)

Infection

Increased susceptibility to infections
• Impaired ability to eliminate invading bacteria, deficient
production of antibodies, and immunosuppressive
effect of many antiinflammatory drugs


Pneumonia is most common infection
No live vaccines if treated with corticosteroids or
cytotoxic drugs
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177
Case Study (1 of 7)
J.C. is a 36-year-old female who was diagnosed
with SLE 8 years ago. Her chart noted polyarthritis,
facial and palmar erythema, and general malaise
as symptoms.
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178
Case Study (2 of 7)
She was started on prednisone 100 mg/every
other day but developed Cushing syndrome within
several weeks.
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179
Case Study (3 of 7)
J.C. later developed intermittent tonic-clonic (grand
mal) seizures that are treated with phenytoin
(Dilantin). During the past year, her lab studies
indicate early kidney failure.
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180
Case Study (4 of 7)
She has had occasional UTIs that have responded
to treatment.

How might this disease be affecting the life of a
36-year-old woman?
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181
Diagnostic Studies


See Table 64-5 in the textbook
No specific test; SLE is diagnosed based on distinct
criteria
 History and physical examination
 Antibodies: ANA is present in 97%
 CBC
 Serum complement
 Urinalysis
 X-rays of affected joints and chest x-ray
 ECG
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182
Interprofessional Care (1 of 3)


Major challenge to manage active disease yet
prevent treatment complications that cause tissue
damage
Survival influenced by:


Age, race, gender, socioeconomic status, co-morbid
conditions, and severity of disease
Early diagnosis and effective treatment
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183
Interprofessional Care (2 of 3)

Drug therapy

NSAIDs
• Mild joint pain

Antimalarial drugs
• Fatigue, skin and joint problems; reduce flares

Corticosteroids
• Severe cutaneous SLE

Immunosuppressive drugs
• Suppress immune system and decrease end-organ
damage
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184
Interprofessional Care (3 of 3)

Topical immunomodulators


Serious skin conditions
Disease management is monitored by serial antiDNA titers and serum complement


See Table 64-16 in the textbook
ESR or CRP
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185
Nursing Assessment (1 of 6)


See Table 64-17 in the textbook
Subjective data
 Past health history
• Exposure to UV light, drugs, chemicals, or viruses;
stress; increased estrogen activity; Pattern of
remissions and flares
 Medications:
• Oral contraceptives, procainamide, hydralazine,
isoniazid, antiseizure meds, antibiotics, corticosteroids,
NSAIDs
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186
Nursing Assessment (2 of 6)

Functional health patterns
• Health perception–health management

Family history, frequent infections, malaise, impact on
functional ability
• Nutrition–metabolic

Weight loss, ulcers, nausea and vomiting, dry mouth,
dysphagia, photosensitivity, infections
• Elimination

Decreased urine output, constipation or diarrhea
• Activity–exercise

Morning stiffness, joint swelling and deformity, dyspnea,
fatigue
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187
Nursing Assessment (3 of 6)

Functional health patterns
• Sleep–rest

Insomnia
• Cognitive–perceptual

Vision problems; vertigo; headache; arthralgia; chest pain;
abdominal pain; fingers cold, painful, numb, and tingly
• Sexuality–reproductive

Amenorrhea, irregular menses
• Coping–stress tolerance

Depression, withdrawal
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188
Nursing Assessment (4 of 6)

Objective data
• General

Fever, lymphadenopathy, periorbital edema
• Integumentary

Alopecia, dry scalp, keratoconjunctivitis, butterfly rash,
palmar or discoid erythema, hives, erythema of nails,
purpura, petechiae, leg ulcers
• Respiratory

Pleural friction rub, decreased breath sounds
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189
Nursing Assessment (5 of 6)

Objective data
• Cardiovascular

Vasculitis, pericardial friction rub, HTN, edema, dysrhythmias,
murmurs, Raynaud’s
• Gastrointestinal

Oral and pharyngeal ulcers; splenomegaly
• Neurologic

Facial weakness, peripheral neuropathies, papilledema,
dysarthria, confusion, hallucination, disorientation, psychoses,
seizure, aphasia, hemiparesis
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190
Nursing Assessment (6 of 6)

Objective data
• Musculoskeletal

Myopathy, myositis, arthritis
• Urinary

Proteinuria
• Possible diagnostic findings





Anti-DNA, Anti-Sm, ANA
Anemia, leukopenia, thrombocytopenia
Elevated ESR, serum creatinine
Hematuria, casts in urine
Pleural effusion or pericarditis
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191
Nursing Diagnoses




Fatigue
Impaired tissue integrity
Difficulty coping
Also see eNursing Care Plan 64-2 on the Evolve
website
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192
Case Study (5 of 7)

What psychosocial issues do you think J.C.
might have that you should be prepared to
discuss with her?
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193
Planning

Overall goals



Have acceptable pain management
Show awareness of and avoid activities that worsen
disease
Maintain optimal role function and positive self-image
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194
Nursing Implementation (1 of 7)

Unpredictable nature of SLE presents many
challenges for the patient and caregiver
 Physical,
psychologic, and sociocultural problems
require long-term management from
interprofessional team
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195
Nursing Implementation (2 of 7)

Disease flare—patient may quickly become very ill


Assess: fever, limitation of motion, location and
degree of discomfort, and fatigue
Monitor weight and Input and Output
• Corticosteroids


Collect 24-hour urine
Observe for bleeding
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196
Nursing Implementation (3 of 7)

Assess neurologic status
 Visual
problems, headaches, seizures,
personality changes, memory loss, psychosis,
peripheral neuropathy

Patient education (see Table 64-18 in the
textbook)
 Explain
nature of disease, treatments, and
diagnostic procedures
 Drug therapy—use, administration, side effects
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197
Nursing Implementation (4 of 7)



Emphasize importance of patient involvement for
successful home management
Help patient understand that strong adherence to
treatment is no guarantee against flares
Reduce exposure to precipitating factors (see Table
64-18 in the textbook)
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198
Nursing Implementation (5 of 7)

Lupus and Pregnancy

SLE common in women of childbearing age;
pregnancy/treatment during pregnancy must be
addressed
• Infertility may have occurred from renal involvement,
high-dose corticosteroids, and immunosuppressive
drugs
• Spontaneous abortion, stillbirth, and intrauterine growth
retardation are common
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199
Nursing Implementation (6 of 7)

Renal, CV, respiratory, and central nervous systems
may be affected during pregnancy
• If already present, counsel against pregnancy


Plan pregnancy when disease activity is minimal
Flares are common postpartum
• Therapeutic abortion does not reduce risk of flare
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200
Nursing Implementation (7 of 7)

Psychosocial issues

Supportive therapies important to cope with the
disease
• Inform patient and caregiver that SLE has good
prognosis for most people
• Stress importance of planning recreational and
occupational activities
• Assist patient in developing goals
• Pregnancy and sexual counseling
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201
Case Study (6 of 7)

What patient teaching might J.C. need?
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202
Case Study (7 of 7)

What resources are available in your community
for patients like J.C. with chronic, often
debilitating, illnesses?
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203
Evaluation

Expected outcomes




Use energy-conservation techniques
Adapt lifestyle to current energy
Maintain skin integrity with the use of topical
treatments
Prevent disease flare with the use of sunscreens and
limited sun exposure
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204
Audience Response Question
(1 of 2)
A patient is undergoing diagnostic testing for symptoms of
polyarthralgia, fatigue, and hair loss. Laboratory results
include the presence of anti-DNA, antinuclear antibodies,
and anti-Smith in the blood. The nurse recognizes that
these findings are most likely to be related to which
diagnosis?
a. Systemic sclerosis
b. Rheumatoid arthritis
c. Chronic fatigue syndrome
d. Systemic lupus erythematosus
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205
Audience Response Question
(2 of 2)
Answer: D
Systemic lupus erythematosus
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206
Reflection Question
SLE can affect women of childbearing age. If she
has a serious form of the disease, childbearing is
discouraged. What might it be like to have to tell
someone she cannot have children?
 How will you approach having such a
conversation?
 What can/should you do?
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207
Scleroderma
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208
Scleroderma (Systemic sclerosis)

Connective tissue disorder characterized by
fibrotic, degenerative, and sometimes,
inflammatory changes in the skin, blood vessels,
synovium, skeletal muscle, and internal organs
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209
Scleroderma (1 of 2)





Occurs in all ethnic groups
More common in blacks, Native Americans, and
people of Japanese descent
Usual age of onset is 30 to 50 years
Rare; 300,000 Americans have disease
Incidence: women four times greater than men
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210
Scleroderma (2 of 2)

Types:


Localized: more common, better prognosis. Skin
changes limited to few places; does not involve trunk
or internal organs
Systemic: rapidly progressive skin and connective
tissue changes with internal organ involvement
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211
Scleroderma
Etiology and Pathophysiology




Exact cause unknown; believed to develop due
to immunologic and vascular abnormalities
Overproduction of collagen (see Fig. 64-11 in the
textbook) causes progressive tissue fibrosis and
blood vessel occlusion
Disrupts function of lungs, kidneys, heart, and GI
tract
Vascular problems involving the small arteries
and arterioles occur early
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212
Clinical Manifestations (1 of 7)


Range from benign limited skin disease to
diffuse thickening with rapidly progressive and
widespread organ involvement
CREST syndrome: localized disease
 Calcinosis
 Raynaud’s
phenomenon
 Esophageal dysfunction
 Sclerodactyly
 Telangiectasis
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213
Clinical Manifestations (2 of 7)

Raynaud’s phenomenon

First problem with localized disease
• May precede onset of systemic disease by months, years, or
decades

Sudden vasospasm of digits leading to:
• Blanching or white phase (decreased blood flow to fingers
and toes when exposed to cold) followed by
• Blue phase (cyanosis as hemoglobin releases O2 to tissues)
and then
• Red phase (rewarming)
• Often see numbness and tingling
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214
Clinical Manifestations (3 of 7)

Skin and joint changes

Symmetric, painless swelling or thickening of the
fingers and hands may progress to diffuse
scleroderma of the trunk
• Localized: doesn’t extend above elbow or knee; may
involve face
• Diffuse: loss of elasticity of skin; taut and shiny skin
causing expressionless face with tightly pursed lips
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215
Clinical Manifestations (4 of 7)

Skin and joint changes

Facial changes may contribute to reduced ROM of
temporomandibular joint
 Sclerodactyly: semi-flexed position of fingers with
tight skin to wrist (see slide 218)
 Reduced peripheral joint function: early symptom of
arthritis
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216
Sclerodactyly in the Hand
(Fig. 64-12)
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217
Clinical Manifestations (5 of 7)

Internal organ involvement

Sjögren’s syndrome: dry eyes and mouth; 20% with
systemic disease
• Dysphagia, gum disease and dental decay
• Esophageal fibrosis can cause gastric acid reflux

Hypomotility of esophagus and dysphagia can lead to
decreased food intake and weight loss
• Constipation from colonic hypomotility
• Diarrhea due to bacterial overgrowth
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218
Clinical Manifestations (6 of 7)

Internal organ involvement

Lungs: pleural thickening, pulmonary fibrosis, and
abnormal function
• Cough and dyspnea develop
• Pulmonary artery HTN and interstitial lung disease
• Lung disease is main cause of death

Heart: pericarditis, pericardial effusion, dysrhythmias
• Heart failure and myocardial fibrosis
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219
Clinical Manifestations (7 of 7)

Internal organ involvement

Renal disease: previously a main cause of death but
treatment has improved
• Malignant HTN can cause progressive, irreversible
renal insufficiency
• Early recognition and treatment needed


Dialysis, bilateral nephrectomy, transplant
ACE inhibitors
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220
Scleroderma
Diagnostic Studies

Blood studies
 Mild,
hemolytic anemia
 Anticentromere antibodies
 Antibodies to topoisomerase-1
 Elevated creatinine

Urinalysis
 Proteinuria,


hematuria, casts
X-rays
Pulmonary function tests
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221
Interprofessional Care

Drug therapy



See Table 64-19 in the
textbook
Vasoactive agents
• Calcium channel blockers
• Angiotensin II blocker
• -adrenergic blocking
agent
• Endothelin-receptor
antagonist
• Vasodilator

Other therapies




Diarrhea—tetracycline
Esophageal symptoms—H2
receptor blockers and
proton pump inhibitors
HTN with renal
involvement—
antihypertensives
Immunosuppressant drugs
NSAIDs and topical
analgesia
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222
Nursing Management (1 of 2)



Time of diagnosis
 Assess: VS, weight, input and output,
respiratory and bowel function, and joint ROM
 Avoid stress and cold ambient temperatures
Psychologic support, biofeedback training, and
relaxation
Sexual counseling
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223
Nursing Management (2 of 2)

Patient education











No finger-sticks with Raynaud’s phenomenon
Exercise program
Moist heat or paraffin baths
Assistive devices
Protect hand and feet from cold
Smoking cessation
Report infection immediately
Alcohol-free lotions
Reduce dysphagia and heartburn
Occupational alterations
Oral hygiene
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224
Polymyositis and
Dermatomyositis
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225
Polymyositis (PM) and
Dermatomyositis (DM) (1 of 8)


Polymyositis: diffuse, idiopathic, inflammatory myopathy
of striated muscle
Dermatomyositis: muscle changes of polymyositis with
skin changes

Rare disorders
 Affect adults older than 20 years
 Women two times more than men
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226
PM and DM (2 of 8)

Etiology and pathophysiology



Exact cause unknown
Autoimmune origin with T-cell mediated destruction of
unidentified muscle antigens
Environmental factors may contribute
• Viral and bacterial infection
• Drugs, supplements, vaccines, medical implants
• Occupational exposure
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227
PM and DM (3 of 8)

Clinical manifestations and complications

Muscular
• Weight loss
• Fatigue
• Muscle weakness in the shoulders, legs, arms, and
pelvic girdle


Difficulty performing routine activities and repetitive
movements
Unable to move against resistance or gravity
• Dysphagia and dysphonia due to weak pharyngeal
muscles
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228
PM and DM (4 of 8)

Dermal
• Rashes: classic red or purple symmetric rash with edema
around eyelids
• Gottron’s papules: knuckles and side of hands (see Fig. 6413 in the textbook)
• Gottron’s sign: interphalangeal spaces
• Poikiloderma: back, buttocks, v-shaped area of anterior neck
and chest
• Nailbeds: hyperemia and telangiectasia
• Calcinosis cutis
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229
PM and DM (5 of 8)

Other manifestations
• Joint redness, pain, and inflammation cause
limited ROM
• Contractures and atrophy (late)
• Poor cough, dysphagia, risk of aspiration
• Interstitial lung disease
• Increased risk of cancer; need screenings
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230
PM and DM (6 of 8)

Diagnostic studies





Muscle biopsy
MRI
Elevated muscle enzymes
EMG
Elevated ESR or CRP
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231
PM and DM (7 of 8)

Nursing and Interprofessional Management


Drug therapy
• Initial treatment: high-dose corticosteroids; taper if
tolerated
• Immunosuppressive drugs
• IV immunoglobulin (see Drug Alert in the textbook)
• Synthetic ACTH
PT
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232
PM and DM (8 of 8)

Patient education






Disease, prescribed therapies, diagnostic studies,
and regular care
Reduce fall risk; use of assistive devices
Reduce risk of aspiration
Energy conservation with activities
Daily exercises/ROM
Home care and bed rest with acute PM
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233
Mixed Connective Tissue Disease

Combination of clinical features of several
rheumatic diseases



SLE, scleroderma, and PM
Affects women in 20s to 30s
Overlap syndrome
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234
Sjögren’s Syndrome (1 of 4)

Common autoimmune disease that targets
moisture-producing exocrine gland
 Xerostomia
and keratoconjunctivitis sicca
 Other glands in stomach, pancreas, and
intestines


Affects people over age 40
Women 10 times more than men
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235
Sjögren’s Syndrome (2 of 4)

Primary Sjögren’s syndrome

Lacrimal and salivary symptoms
• 20% to 40% also have lung, liver, kidneys, and skin
involvement
• Increased risk for non-Hodgkin’s lymphoma

Etiology: genetic and environmental
• Genes: Whites; Japanese, Chinese, African American
• Trigger: viral or bacterial infection; lymphocytes attack
lacrimal and salivary glands
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236
Sjögren’s Syndrome (3 of 4)

Manifestations

Dry eyes: burning, blurred vision, photosensitivity
 Dry mouth: buccal fissures, change in taste, dysphagia,
mouth infections, dental decay
 Other: dry skin, rashes, joint and muscle pain, and thyroid
problems (e.g., Grave’s disease and Hashimoto’s
thyroiditis)
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237
Sjögren’s Syndrome (4 of 4)


Ophthalmologic exams: Schirmer’s test
Treatments:
 Dry
eyes
• Artificial tears or ointment; antiinflammatory drops
• Surgical punctal occlusion
• Increased fluid intake
 Dry
mouth
• Pilocarpine and cevimeline
• Increased humidity
• See Safety Alert in the textbook: to help with chewing or
swallowing
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238
Myofascial Pain Syndrome
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239
Myofascial Pain Syndrome (1 of 3)

Chronic muscle pain and tenderness


Referred pain to:



Chest, neck, shoulders, hips, and lower back
Buttock, hand, and head
Can cause temporomandibular joint (TMJ) pain
Occurs most with middle-aged adults and women
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240
Myofascial Pain Syndrome (2 of 3)


Pain within connective tissue that covers skeletal
muscles
Trigger or tender points



Activated by pressure
Worsens with activity or stress
Deep, aching pain accompanied by burning,
stinging, stiffness
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241
Myofascial Pain Syndrome (3 of 3)

Treatment

Physical therapy
• “Spray and stretch” method—painful area is iced or
sprayed with a coolant and then stretched

Topical patches
 Trigger point injections
 Massage, acupuncture, biofeedback, ultrasound
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242
Fibromyalgia
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243
Fibromyalgia (1 of 2)

Chronic central pain syndrome



Widespread, nonarticular musculoskeletal pain and
fatigue
Multiple tender points
Also have:




Nonrestorative sleep
Morning stiffness
Irritable bowel syndrome
Anxiety
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244
Fibromyalgia (2 of 2)






Common disorder
Major cause of disability
Affects 3.7 million in United States
More common in women ages 40 to 75 years
Many shared features with systemic exertion
intolerance disease (SEID)
See Table 64-20 in the textbook
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245
Fibromyalgia
Etiology and Pathophysiology


Abnormal central processing nociceptive pain input due
to abnormal sensory processing in CNS
Multiple physiologic abnormalities:







Increased levels of substance P in spinal fluid
Low blood flow to thalamus
Dysfunction of hypothalamic-pituitary-adrenal (HPA) axis
Low levels of serotonin and tryptophan
Abnormalities in cytokine function
Genetics
Recent illness or trauma
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246
Fibromyalgia: Clinical
Manifestations and Complications
(1 of 4)




Widespread burning pain that fluctuates
throughout day
Trouble determining if pain is in muscles, joints,
or soft tissues
Head or facial pain
Can accompany TMJ dysfunction
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247
Case Study (1 of 8)
A.S., a 45-year-old female, comes to the clinic for
widespread burning pain that worsens and
improves throughout the day. She also reports
being very tired. Her medical history is negative
except for irritable bowel syndrome.
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248
Case Study (2 of 8)

What factor(s) in A.S.’s initial presentation
suggest(s) she may be suffering from
fibromyalgia instead of myofascial pain
syndrome?
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249
Case Study (3 of 8)

What specific areas will you palpate for point
tenderness in A.S.?
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250
Tender Points in Fibromyalgia





Physical examination
Point tenderness in 11 of
18 sites
Pain throughout body
Pain from unusual
stimulus (allodynia)
Pain varies day to day

Sometimes fewer than
11 sites
 Sometimes all sites
Fig. 64-14
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251
Case Study (4 of 8)

What other clinical manifestations will you
assess for in A.S.?
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252
Fibromyalgia: Clinical
Manifestations and Complications
(2 of 4)

Cognitive effects




Range from difficulty concentrating to memory lapses
Feelings of being overwhelmed when dealing with
multiple tasks
Migraine headaches
Depression and anxiety
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253
Fibromyalgia: Clinical
Manifestations and Complications
(3 of 4)





Stiffness
Nonrefreshing sleep
Fatigue
Paresthesia in hands and feet
Restless legs syndrome
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254
Fibromyalgia: Clinical
Manifestations and Complications
(4 of 4)




Irritable bowel syndrome
Difficulty swallowing
Greater frequency of urination and urinary
urgency
For women, difficult menstruation with increased
disease symptoms
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255
Case Study (5 of 8)

What diagnostic studies would you anticipate the
health care provider ordering?
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256
Fibromyalgia
Diagnostic Studies (1 of 3)



Definitive diagnosis difficult
Laboratory results rule out other suspected
disorders
Muscle biopsy


Nonspecific moth–eaten appearance
Fiber atrophy
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257
Case Study (6 of 8)
A.S.’s lab work results are all within normal limits.
The health care provider diagnoses her with
fibromyalgia.
 What criteria would the health care provider use
to support the diagnosis of fibromyalgia?
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258
Fibromyalgia
Diagnostic Studies (2 of 3)

ACR: Fibromyalgia if 2 criteria are met:



Pain is experienced in 11 of 18 tender points on
palpation (see Fig. 64-14 in the textbook)
History of widespread pain is noted for at least 3
months
Fatigue, cognitive symptoms, somatic symptoms
help establish diagnosis
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259
Fibromyalgia
Diagnostic Studies (3 of 3)

Subsequent classification by ACR

Nontender point diagnostic criteria
• Symptom severity scale
• Widespread pain index

Use with previous ACR criteria
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260
Fibromyalgia
Interprofessional Care (1 of 2)




Symptomatic treatment
Requires high level of patient motivation
Patient teaching
Rest
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261
Case Study (7 of 8)
A.S. tells you she is glad that she finally knows
what is wrong with her. She is anxious to begin her
medications to help her feel better.
 What drug treatments might you anticipate the
health care provider ordering for A.S.?
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262
Fibromyalgia
Interprofessional Care (2 of 2)

Drug therapy for chronic widespread pain







Pregabalin (Lyrica)
Duloxetine (Cymbalta)
Milnacipin (Savella)
Low-dose tricyclic antidepressants (TCAs), SSRIs,
or benzodiazepines
Muscle relaxants
OTC and nonopioid analgesics
Zolpidem (Ambien)
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263
Case Study (8 of 8)

What other treatments and/or interventions
would you include in your teaching to A.S.?
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264
Fibromyalgia
Nursing Management (1 of 2)






Supportive care
Massage combined with ultrasound
Application of alternating heat and cold packs
PT (gentle stretching)
Yoga/Tai Chi
Low impact aerobic exercise
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265
Fibromyalgia
Nursing Management (2 of 2)

Limit intake of sugar, caffeine, alcohol




May be muscle irritants
Vitamin and mineral supplements
Avoid “miracle” diets and supplements
Relaxation strategies


Biofeedback, imagery, meditation, cognitive
behavioral therapy
Psychologic counseling and support group
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266
Systemic Exertion Intolerance
Disease
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267
Systemic Exertion Intolerance
Disease (SEID)


Formerly: chronic fatigue syndrome
Complex, multisystem disease


Affects at least 1 million people in United States



Physical, emotional, or cognitive exertion impaired
and accompanied by profound fatigue
Many undiagnosed
Women 3 to 4 times more than men
Affects all ethnicities; more common in minorities
and socioeconomically disadvantaged
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268
SEID
Etiology and Pathophysiology


Precise mechanisms remain unknown
Many theories exist about cause

Neuroendocrine abnormalities involving a
hypofunction of HPA axis and hypothalamic-pituitarygonadal (HPG) axis
 Several microorganisms investigated
 Changes in CNS
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269
Case Study (1 of 5)
D.L. is a 32-year-old female who visits her health
care provider reporting severe fatigue for the past
6 months. She states that rest does not help.
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270
Case Study (2 of 5)
She also says she has general malaise and an
inability to concentrate. She has needed to ask her
sister to help her around the house and drive her
kids to school.
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271
Case Study (3 of 5)

What clinical manifestations of systemic exertion
intolerance disease does D.L. have?

What other manifestations will you assess for
with D. L.?
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272
SEID
Clinical Manifestations (1 of 2)

Diagnosis requires 3 symptoms:




Impaired function with profound fatigue lasting at least
6 months
Postexertional malaise
Unrefreshing sleep
Plus at least 1 of the following:


Cognitive impairment (“brain fog”)
Orthostatic intolerance
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273
SEID
Clinical Manifestations (2 of 2)


Severe fatigue: most common symptom and reason patient
seeks health care
Difficult to distinguish from fibromyalgia


Slow onset or intermittent episodes that become chronic



See Table 64-20 in the text
May be triggered by flu-like illness or acute stress
Associated symptoms may vary in intensity
Patients feel angry and frustrated at lack of diagnosis; impacts
work and family responsibilities
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274
Case Study (4 of 5)
D.L.’s HCP suspects SEID.
 Are there any diagnostic studies useful for
confirming SEID?
 How will the HCP establish this diagnosis?
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275
SEID
Diagnostic Studies



Physical examination and diagnostic studies rule
out other possibilities
No laboratory test can diagnose or measure
severity
In general, a diagnosis of exclusion
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276
Case Study (5 of 5)
The HCP prescribes treatment for SEID for A.L.

What treatments and other interventions
appropriate for SEID will you discuss with A.L.?
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277
SEID: Interprofessional
Management (1 of 4)



Supportive management
Patient teaching about SEID
Drug therapy





NSAIDs
Antihistamines/decongestants
Tricyclic antidepressants and SSRIs
Clonazepam (Klonopin)
Low-dose hydrocortisone
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278
SEID: Interprofessional
Management (2 of 4)

Activity




Avoid total rest
Strenuous exertion can exacerbate exhaustion
Gradual exercise program
Well-balanced diet


Fiber
Dark-colored fruits and vegetables
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279
SEID: Interprofessional
Management (3 of 4)

Behavioral therapy

Loss of livelihood and economic security



Cannot work or decreased time working
Loss of job leads to loss of medical insurance
Obtaining disability benefits may be frustrating/difficult
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280
SEID: Interprofessional
Management (1 of 4)

Severe occupational and psychosocial loss; social
pressure and isolation


Labeled lazy or crazy
SEID does not appear to progress

Most patients recover or gradually improve over time
 Some do not show significant improvement
 Recovery more common with sudden onset
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281
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