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Overview of Rheumatoid Arthritis
Paula Ellsworth RN, BSN
University of Cincinnati
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Abstract
Rheumatoid arthritis (RA) causes functional disability reducing quality of life in those
affected. The overall goal of management is to reduce pain and inflammation preventing further
joint destruction. There are a variety of treatments available that can reduce the effects RA. It is
important to refer patients with suspected RA to a rheumatologist as soon as possible. Early
treatment is essential for maintaining quality of life and prevention of joint damage. The purpose
of this article is to give a comprehensive overview of RA and help guide nurse practitioners in
diagnosis, treatment, and management in this patient population.
Keywords: rheumatoid arthritis, pathophysiology, risk factors, presentation, management
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Introduction
In 2005, an estimated 1.29 million adults in the United States (US) were diagnosed with
Rheumatoid arthritis (RA) [13]. RA has been diagnosed in all ethnic groups and affects 1% of
the world’s population [13]. RA is a devastating disease that is life long and has potentially
disabling consequences. It affects women more than men and typically begins between the fourth
and sixth decade of life; however, it can develop at any age [2, 13]. RA is a chronic, progressive,
systemic inflammatory autoimmune disease associated with swelling and pain in multiple joints,
eventual joint destruction, functional disability, and a reduced quality of life [13]. The overall
goal of management is to reduce pain and inflammation and prevent further joint destruction.
Studies have shown that 37% of patients with RA are unable to work within 2 years of diagnosis
and 17% undergo joint surgery after a median of 3 years [1]. There are a variety of treatments
available that can reduce the effects of this disease. These therapies can slow and, in some cases,
stop the progression of RA. It is important to refer patients with suspected RA to a
rheumatologist as soon as possible. RA has a gradual onset, but damage starts early. Early
treatment is essential for maintaining quality of life and prevention of joint damage.
Epidemiology
RA is a chronic, progressive, systemic inflammatory autoimmune disease that affects
synovial joints [11]. RA is the most common form of inflammatory arthritis [14]. Etiology of RA
is not fully understood. Evidence points to environmental and genetic risk factors [3]. Prevalence
of RA increases with age and is two to three times more common in women than in men [2, 4,5].
RA involves joints bilaterally, most typically affecting the small joints in hands, wrists, and feet.
As the disease progresses it can also affect the mandibular joints, cervical spine, shoulders,
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elbows, hips, knees and ankles [9]. RA affects the lining of joints, causing a painful swelling that
can eventually result in bone loss and joint deformity [7, 8].
Etiology and Pathophysiology
RA, like many autoimmune diseases, has a multifaceted etiology. Evidence points to a
complex relationship between genetic and environmental risk factors. Pathogenesis of RA is as
follows: antigens are triggered by environmental or infectious agents, genetic susceptibility
activate T lymphocytes (also known as T cells) promoting cytokine release and activating B
lymphocytes, T cells stimulate synovial macrophages and fibroblasts which then activate B
lymphocytes causing formation of rheumatoid factor (RF) [2].
Joint damage in RA begins with proliferation of synovial macrophages and fibroblasts
after a triggering incident, possibly autoimmune or infectious. Lymphocytes infiltrate
perivascular regions and endothelial cells proliferate. Neurovascularization then occurs. Blood
vessels in the affected joint become occluded with small clots or inflammatory cells. Over time
synovial tissue begins to grow irregularly, forming invasive pannus tissue. Pannus invades and
destroys cartilage and bone [9, 10]. Overproduction of multiple inflammatory cytokines,
including tumor necrosis factor (TFN) and interleukin-6, are released causing further joint
destruction and development of systemic complications [10, 14].
Risk Factors
Risk factors are both environmental and genetic. The strongest genetic association with
RA is the human leucocyte antigen (HLA), particularly the HLA-DRB1 (death receptor beta)
‘shared epitope’ with two copies associated with relative risk of developing RA [3]. Various
environmental risk factors have been implicated in RA: female sex, family history, older age,
silicate exposure, and smoking [10]. There is evidence that supports exposure to infectious
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agents: bacteria, mycoplasmas, and viruses. Viruses such as Epstien-Bar virus (EBV), Parvovrius
B19, and bacteria including Streptococcus, Mycoplasma, Proteus and Escherichia coli [3]. High
vitamin D intake, tea consumption, and oral contraceptives are associated with decreased risk for
RA [10]. Pregnancy often improves symptoms of RA and may even cause remission; this may be
attributed to immunologic tolerance; however recurrence usually happens after delivery [10, 14].
Typical Presentation
Patients with RA present with pain and stiffness in multiple joints [10, 14]. Joints commonly
affected are those with the highest ratio of synovium to articular cartilage [10]. The wrists, proximal
interphalangeal joints, and metacarpophalangeal joints are almost always involved [10, 14]. The affected
joints stiffen upon rising in the morning usually lasting more than one hour and worsen with
inactivity suggesting an inflammatory etiology [14]. Patients often report general symptoms, such as
morning stiffness, fatigue, fever, sweats, and weight loss [2, 7, 9, 10, 14]. Palpation of joints may reveal
swelling within the joint, sometimes with bulging and pain on pressure [7]. Rheumatoid joints are boggy,
tender to the touch, and warm, but usually are not erythematous [10]. Movement is limited particularly in
extension or rotation, and force is reduced, resulting in difficulty for the patient to make a fist. Heat and
redness may be present, but absence of these signs does not preclude inflammation. In later stages of
disease, rheumatic nodules or deformation might be seen, typically with ulnar deviation of the
metacarpophalangeal joints [7].
Diagnostic Tests
No single diagnostic test is able to definitively confirm the diagnosis of RA. There are
several tests that can provide objective data for the differential diagnosis of RA. Evaluating
laboratory results and imaging studies are important in diagnosing and monitoring the
progression of this disease. The American College of Rheumatology Subcommittee on
Rheumatoid Arthritis (ACRSRA) recommends that baseline laboratory evaluations include a
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complete blood count (CBC) with differential, Rheumatoid factor (RF), erythrocyte
sedimentation rate (ESR) or C-reactive protein (CRP). Baseline evaluation of renal and hepatic
function is also recommended because these findings will guide medication choices
[10].Aspiration of synovial fluid may be considered if joint can be tapped and diagnosis is
uncertain [10].
X-rays of both hands and wrists are used to stage the disease and prognosis [4, 9]. X-rays
in the early stages would note bone demineralization and soft tissue swelling; which progresses
to loss of cartilage, and narrowing of the joint spaces; finally, cartilage and bone destruction,
erosion, subluxation, and deformities occur [4, 9, 10]. Typical findings in RA, show an elevated
RF level, which is found in 50-80% of people with RA [14]. ESR and CRP are often increased in
active RA [9, 14]. ESR and CRP levels can be used to follow disease activity and response to
medication. CBC with differential and renal and hepatic function results would influence
treatment choices [14]. Synovial fluid analysis would reveal straw colored fluid, fibrin flecks,
leucocytes, polymorphonuclear leucocytes and complement [9, 10].
Classification Criteria for RA
Until 2010 the 1987 American College of Rheumatology (ACR) classification criteria
was used to diagnosis RA, but this criteria was criticized for its lack of sensitivity in early
disease. The new criterion was developed by the ARC and the European League Against
Rheumatism Collaborative Initiative (EULAR). These new classification criteria can be applied
to any patient as long as two mandatory requirements are fulfilled; 1) at least one joint with
definite clinical synovitis (swelling), 2) synovitis not explained by another disease [1].
Examples of other diseases are: systemic lupus erythematosis, psoriatic arthritis, and gout. Four
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additional criteria can be applied to eligible patients: 1) joint involvement, 2) serology, 3) acutephase reactants, and 4) duration of symptoms. The following is an example of the additional
criteria [1]:
Joint involvement
1 large joint
2-10 large joints (shoulders, elbows, hips, knees, ankles)
1-3 small joints (with or without involvement of large joints)
4-10 small joints (with or without involvement of large joints)
>10 joints (at least 1 small joint)
0
1
2
3
5
Serology (at least 1 test result is needed for classification)
Negative RF and
negative autoantibodies against citrullinated antigens (ACPA)
Low-positive RF or low-positive ACPA
High-positive RF or high-positive ACPA
0
2
3
Acute-phase reactants (at least 1 test result is needed for classification)
Normal CRP and normal ESR
0
Abnormal CRP or abnormal ESR
1
Duration of symptoms
< 6 weeks
>6 weeks
0
1
For a patient to be considered to have RA, 6 points out of 10 are necessary to meet criteria [1].
The ACR/EULAR classification criteria for RA presents a new approach with specific emphasis
on identifying patients that have had symptoms for a short period of time, and who may benefit
from early initiation of DMARDs [1]. The 1987 ACR criteria for classification of RA are as
follows:

Morning stiffness lasting at least at 1 hour

Soft tissue swelling in three or more joints

Swelling of proximal interphalangeal, metacarpophalangeal, or wrist joints
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
Symmetric distribution

Subcutaneous nodules

Positive rheumatoid factor

Radiographic erosions or periarticular osteopenia in hand or wrist joints
Four or more of these are necessary for a diagnosis of RA [7, 9]. It is easy to see the advantages
of the new RA classification system in early diagnosis and prevention of damage and
complications that accompany this disease process.
Management and Treatment of RA
The overall goals of management are to reduce pain and inflammation preventing further
joint destruction. Therapeutic goals are directed at preservation of function and quality of life,
minimization of pain and inflammation, joint protection, and control of systemic complications
[10]. Treatment should be guided by individual clinical response to various interventions. The
ACRSARA recommends patients with suspected RA be referred to a rheumatologist within three
months of presentation for confirmation of diagnosis and initiation of treatment [10]. General
management consists of supportive measures such as encouraging your patient to get 8-10 hours
of sleep per night along with frequent rest periods between daily activities. Splinting inflamed
joints, physical therapy programs that include range of motion exercises, and carefully
individualized therapeutic exercise can forestall loss of joint function. Application of heat
relaxes muscles and relieves pain. Moist heats works best for those with chronic pain and ice
packs can be encouraged for acute episodes [9]. Alternative methods used consist of
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hydrotherapy, biofeedback, meditation, acupressure, acupuncture, yoga, hypnosis, and massage.
These methods may produce a sense of psychological well-being and relaxation [9].
Subsequent management is achieved with medications. Medications used in the treatment
of RA are nonsteriodial anti-inflammatory drugs (NSAIDs), corticosteroids, and disease
modifying ant-rheumatic drugs (DMARDs). NSAIDs help decrease the inflammatory response
and improve the patient’s level of pain and function. Intra-articular injections of corticosteroids
are sometimes beneficial when a patient has joint inflammation, swelling, and pain. Some
patients may also require oral or intravenous (IV) corticosteroids if joint inflammation is severe.
To slow the progression of RA, DMARDs may be prescribed. A combination of DMARDs and
NSAIDs can be used when joint inflammation and swelling are persistent [9]. DMARDs are a
genetically engineered class of medications that reduce inflammation and structural damage to
the joints by interrupting the cascade of events that drive inflammation. Early treatment with
DMARD improves both short and long term clinical, radiological, and functional outcomes
compared to delayed treatment [11].
Surgery is used to correct deformity or mechanical deficiency in intermediate or late
stages of RA. Surgery is considered a treatment for RA only when the patient’s pain is
unacceptable, loss of mobility significant, or functional impairment is severe [9]. Surgical
options include: synovectomy, tendon reconstruction, joint reconstruction, joint fusion or total
joint arthroplasty. All are powerful treatment modalities to prevent disability in advanced RA
[9].
Complications of RA
Untreated RA leads to joint destruction, functional limitations, severe disability, and a
reduced life expectancy [4]. Further complications of untreated RA consist of: anemia of
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chronic disease, cancer, cardiac complications, cervical spine disease, eye problems, fistula
formation, increased infections, hand joint deformities, other joint deformities, respiratory
complications, rheumatoid nodules, and vasculitis [10].
Two important complications of RA are cardiovascular disease and osteoporosis. It has
been established that atherosclerosis is more prevalent among patients with RA. Similarities have
been noted between inflammatory pathways operating in atherosclerosis and RA [12]. RA is also
associated with decreased elasticity of the aorta; arterial stiffness may act as a marker for the
development of future cardio vascular disease (CVD). Studies show that there is a correlation
between the duration of RA (greater than 10years) and the presence of aortic stiffness [11].
Ongoing cardiovascular risk assessment is recommended for all RA patients. To reduce risk,
proper control and management of disease activity is mandatory [7]. It is also important to
recognize osteoporosis early in RA. Osteoclasts have been shown to play an important role in the
pathogenesis of RA. RA inflammation results in peri-articular bone loss adjacent to affected
joints as well as generalized axial and appendicular bone loss at sites distant from inflamed
joints. Corticosteroids can also increase the risk for osteoporosis [12].
Depression and RA
Depression is a primary psychological symptom associated with RA. The causes are
related to increased pain, reduced ability to engage in activities of daily living, sleep deprivation,
living with a chronic illness, and lack of a supportive social network. It is important to encourage
counseling and support groups for these patients. Difficulties in sexual performance are usually
related to problems of overall disability and hip involvement, while diminished desire and
satisfaction are influenced by pain, age, and depression. Encourage rest; consider tricyclic
antidepressants, and selective serotonin reuptake inhibitors (SSRIs). RA also affects family
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relationships. The impact of RA can be a financial and social burden on the patient and family.
Encourage patient and family to become involved in self-help groups [9].
Prognosis
It has been reported that patients with RA live three to twelve years less than the general
population. Increased morality is related to accelerated CVD, especially in those with high
disease activity and chronic inflammation [14]. Predictors of poor outcomes in the early stages of
RA include: low functional score in early disease, lower socioeconomic level, lower educational
level, strong family history of disease, and early involvement of joints [10]. Prognosis is worse in
patients who have a high ESR or CRP level at disease onset, positive RF, or early radiographic
changes. Patients with milder disease tend to benefit from early treatment [10]. The new
biological therapies may reverse progression and atherosclerosis and extend the life span in those
with RA [12]. Therapeutic approaches call for early intervention with DMARDs to avoid long
term disability and premature death [6]. Patients with clinical signs and symptoms of RA should
be referred to a rheumatologist as early as possible.
Conclusion
Practitioners should use a team approach to treat patients with RA. This disease has many
additional complications and underlying disease processes that need to be addressed and
education is the key. RA is a lifelong disease with no cure. Supportive measures and a holistic
approach may be needed to help this patient population stay active for as long as possible. It is
important to always keep the goals of medical management of RA in mind. These include: early
diagnosis, early initiation of pharmacological treatment, patient education and counseling,
alleviation of symptoms, suppression of inflammation and structural joint damage, prevention of
joint deformity and dysfunction, maximization of independence and promotion of an active
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lifestyle, continual assessment of disease progression, ongoing evaluation of therapeutic
modalities, assessment and minimization of drug side effects and risks. It is best to utilize
pharmacological modalities, occupational and physical therapy, assistive devices and surgical
interventions to enhance the quality of life in this patient population [2]. It is important to refer
patients early with suspected RA to a rheumatologist as soon as possible. Early treatment is
essential for maintaining quality of life and prevention of joint damage.
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References
Aletaha, D., Neogi, T., Silman, A. J., Funovitis, J., Felson, D. T., Bingham, C. O., . . . Burmester,
G. R. (2010, September). 2010 Rheumatoid arthritis classification criteria. Retrieved
April 1, 2012, from The American College of Rheumatology database.
Capriotti, T. (2007, May). Rheumatoid arthritis. Advance for Nurse Practitioner, 61-67.
Colebatch, A. N., & Edwards, C. J. (2011, January). The influence of early life factors on the risk
of developing rheumatoid arthritis. Clinical and Experimental Immunology, 163(1), 1116.
Davis, L. (2007, October). Primer on arthritis in primary care. The Clinical Advisor, 30-37.
Devine, E. B., Alfonso-Cristancho, R., & Sullivan, S. D. (2011, January). Effectiveness of
Biologic Therapies for Rheumatoid Arthritis: An Indirect Comparison Approach.
Pharmacotherapy, 31(1), 39-51.
Gaujoux-Viala, C., Smolen, J. S., Landewe, R., Dougados, M., Kvien, T. K., Mola, E. M., . . .
van Riel, P. (2010, June). Current evidence for the management of rheumatoid arthritis
with synthetic drugs: a systemic literature review informing the EULAR
recommendations for the management of rheumatoid arthritis. Annels of the Rheumatic
Disease, 69(6), 1004-1009.
Klarenbeek, N. B., Kerstens, P. S., Huizinga, T. W., Dijkmans, B. A., & Allaart, C. F. (2011,
January). Recent advances in the management of rheumatoid Arthritis. British Medical
Journal, 342, 39-44.
Mease, P. J. (2010, August). Improving the Routine Management of Rheumatoid Arthritis: The
Value of Tight Control. The Journal of Rheumatology, 37(8), 1570-1578.
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Pullen, R. L., Edwards, T., & Grove, D. (2008, July/August). Caring for the
patient with rheumatoid arthritis [Better Resources for Better Care].
Retrieved October 13, 2011, from Lippincott's Nursing Center.com database.
Rindfleisch, J. A., & Muller, D. (2005, September). Diagnosis and Management of Rheumatoid
Arthritis. American Family Physician, 72(6), 1037-1047.
Sliem, H., & Nasr, G. (2010, July). Change of the aortic elasticity in rheumatoid arthritis:
Relationship to associated cardiovascular risk factors. Journal of Cardiovascular Disease
Research, 1(3), 110-115.
Suresh, E. (2010, April). Recent advances in rheumatoid arthritis. Postgraduate Medical
Journal, 86(1014), 243-250.
Swanson, K. I., & Pfenning, S. (2011, November/December). The nurse practitioner's role in the
management of rheumatoid arthritis. The Journal for Nurse Practitioners, 7(10), 858870.
Wasserman, A. M. (2011, December). Diagnosis and management of rheumatoid arthritis.
American Family Physician, 84(11), 1245-1252.