Rheumatoid Arthritis

Rheumatoid Arthritis is a chronic, systemic, inflammatory autoimmune disease with unknown

origin that may affect many tissues but principally attacks synovial joints. Inflammation and
thickening of the synovial membranes (the sacs holding the fluid that lubricates the joints) cause
irreversible damage to the joint capsule and the articular (joint) cartilage as these structures.
Incidence
Rheumatoid arthritis is a common rheumatic disease, affecting approximately 1% of the
current population worldwide. The disease is three times more common in women as in men. It
afflicts people of all races equally. The disease can begin at any age and even affects children
(juvenile idiopathic arthritis), but it most often starts after 40 years of age and before 60 years of
age. Though uncommon, in some families, multiple members can be affected, suggesting a
genetic basis for the disorder.
Pathophysiology
Both genetic as well as environmental factors are implicated in the pathophysiology of
the disease. Smoking is the main environmental risk to RA. 50% of the risk of having RA is
attributable to genetic factors. No infectious agent has been consistently linked with RA and
there is no evidence of disease clustering to indicate its infectious etiology.
Precipitating Factor
> Environment
> Smoking

Predisposing Factor
> Age (40-60)
> Gender (F>M)
> Genetics

UNKNOWN ETIOLOGY

Antigen presenting cell in Synovium

T helper cell

Cytokines

Macrophages

Interleukin 6 (IL6)
B cells
IL1, TNF, IL6

Plasma cells
Antibody secretion

Rheumatoid Factor

IgG

Matrix Metalloprotinase (MMP)

effects on bone remodeling

RANKL (osteoblast), OPG

RANKL binds to RANK (preosteoclast)

Against FC of IgG

Immune Complex

Osteoclast

Erosion of bone

Synovial Inflammation

Stiffness
Pain
Swelling
Redness
Warmth
Immobilization

Cartilage Damage

Contractures

Bone Damage

Deformity

Joint Dysfunction

Rheumatoid Nodule

Pannus formation

RA is an autoimmune disease of unknown origin that primarily occurs in the synovial

tissue. An antigen presenting cell activates T helper cell, a type of T cell that have two functions:
Increases bactericidal activity of Macrophages, and the activation of cytokines. Cytokines
specifically Interleukin 6 brings in B cells which differentiates into Plasma cells. Plasma cells in
turn, secretes antibodies including IgG and Rheumatoid Factor - an autoantibody that commonly
found on RA. RF is an antibody against the FC portion of IgG. The presence of Rheumatoid
factors is an integral part of RA disease process. RF and IgG join to form immune complexes.
Once the abnormal immune response has become established (which may take several years
before any symptom occurs), plasma cells continue to produce Antibodies and RF in large
quantities leading to an autoimmune reaction. The antibodies attack synovium leading to
inflammation.
Macrophage on the other hand, produce Matrix Metalloprotinases which breakdowns
extracellular matrix leading to cartilage damage. Macrophage also produces cytokines IL1, IL6,
and TNF which somehow, affects bone remodeling process. Normally, bone breakdown occurs
when Osteoblast receptor RANKL (Receptor Activator of Nuclear Factor kappa-B Ligand) binds
with Preosteoclast RANK (Receptor Activator of Nuclear Factor kappa-B). The binding activates
osteoclast which functions to resorb/breakdown bone tissue. As an inhibitory mechanism,
Osteoblast produce Osteoprotegerin (OPG) which acts as a decoy receptor for RANKL and
inhibits the development of Osteoclast. However, in the disease process of RA, cytokines IL1,
IL6, and TNF produce by macrophages somehow increases RANKL in the synovium while
decreasing OPG. As a result, bone breakdown occurs and later bone erosion.

Both autoimmune reaction and bone erosion causes inflammation in the synovium
leading swelling in joint, pain, stiffness, redness, and warmth leading to immobilization.
Immobilization for extended period of time can lead to contractures, creating soft tissue
deformity. Rheumatoid Nodule, collection of immune cells, also developed when immune
system goes to the inflamed site but unable to eliminate foreign substances. The inflamed
synovium also leads to pannus formation. Pannus is an abnormal layer of fibrovascular tissue or
granulating tissue which invades cartilage leading to bone and cartilage damage. Muscle fibers
undergo degenerative changes, elasticity and power are lost and joint dysfunction occurs.
Clinical Manifestations
Clinical Manifestations of RA vary, usually reflecting the stage and severity of the
disease.RA primarily affects joints, however it also affects other organs in more than 1525% of
individuals Arthritis of joints involves inflammation of the synovial membrane. Joints become
swollen, tender and warm, and stiffness limits their movement. With time, multiple joints are
affected. Most commonly involved are the small joints of the hands, feet and cervical spine, but
larger joints like the shoulder and knee can also be involved. Synovitis can lead to tethering of
tissue with loss of movement and erosion of the joint surface causing deformity and loss of
function
RA typically manifests with signs of inflammation, with the affected joints being
swollen, warm, painful and stiff, particularly early in the morning on waking or following
prolonged inactivity. Increased stiffness early in the morning is often a prominent feature of the
disease and typically lasts for more than an hour. Gentle movements may relieve symptoms in
early stages of the disease. These signs help distinguish rheumatoid from non-inflammatory
problems of the joints, often referred to as osteoarthritis or "wear-and-tear" arthritis. The joints
are often affected in a fairly symmetrical fashion, although this is not specific, and the initial
presentation may be asymmetrical. Systemic symptoms includes generalized fatigue, malaise,
and fever.
Assessment and Diagnostic Findings
Several factors can contribute to a diagnosis of RA: Rheumatoid nodules, joint
inflammation detected on palpation, and laboratory findings. The history and physical
examination addresses manifestation such as bilateral and symmetric stiffness, tenderness,
swelling, and temperature changes in joints. The client is also assessed for weight loss, fatigue
and malaise.
Rheumatoid Factor blood test is also done since RF is an integral part in the disease
process of RA. Erythrocyte sedimentation rate test (ESR) is also performed. It is useful in
detecting inflammation as it measures the speed at which RBC settle to the bottom of an upright
test tube. When theres an inflammation, RBC tends to clump together and sink more quickly
which result in high ESR value. Antinuclear antibody test (ANA) is also tested since it detects
autoantibodies present in an individuals blood serum. C-reactive protein (CRP) is a non-specific
test that detects inflammation if there is high suspicion of tissue injury but the test cannot tell
where the inflammation is or what condition is causing it. Normally, CRP in blood is normally
low. CBC is often used as a broad screening test to determine an individuals general health
status. anti-citrullinated protein antibodies (ACPAs) or anti-CCP test are also performed. ACPA

are autoantibodies against peptides and proteins. Like RF, these tests are positive in only a
proportion (67%) of all RA cases, but are rarely positive if RA is not present, giving it a
specificity of around 95%. As with RF, there is evidence for ACPAs being present in many cases
even before onset of clinical disease. Arthocentesis shows synovial fluid that is cloudy, milky,
or dark yellow and contains numerous inflammatory components such as leukocyte and
complement.
X-rays show bony erosions and narrowed joint spaces. X-rays of the hands and feet
should be performed at baseline to help establish the diagnosis of RA and then every 3 years to
monitor the progression.
In 2010 the 2010 ACR / EULAR Rheumatoid Arthritis Classification Criteria were
introduced. The new criteria is not a diagnostic criteria but a classification criteria to identify
disease with a high likelihood of developing a chronic form. However a score of 6 or greater
unequivocally classifies a person with a diagnosis of Rheumatoid arthritis. It establish a point
value between 0 and 10. Four areas are covered in the diagnosis

joint involvement, designating the metacarpophalangeal joints, proximal interphalangeal

joints, the interphalangeal joint of the thumb, second through fifth metatarsophalangeal
joint and wrist as small joints, and shoulders, elbows, hip joints, knees, and ankles as large
joints:
Involvement of 1 large joint gives 0 points
Involvement of 210 large joints gives 1 point
Involvement of 13 small joints (with or without involvement of large joints) gives 2
points
Involvement of 410 small joints (with or without involvement of large joints) gives 3
points
Involvement of more than 10 joints (with involvement of at least 1 small joint) gives 5
points

serological parameters including the rheumatoid factor as well as ACPA

Negative RF and negative ACPA gives 0 points
Low-positive RF or low-positive ACPA gives 2 points
High-positive RF or high-positive ACPA gives 3 points

acute phase reactants: 1 point for elevated erythrocyte sedimentation rate, ESR, or
elevated CRP value (c-reactive protein)
duration of arthritis: 1 point for symptoms lasting six weeks or longer

Medical Surgical Management

There is no cure for RA, but treatments can improve symptoms and slow the progress of the disease. Patients
with RA should receive aggressive and early treatment. The main treatment goals with rheumatoid arthritis are
to control inflammation and slow or stop the progression of RA. Treatment is usually multifaceted program
that consist of medications, physical therapy, and regular exercise.

Drugs for RA

NSAIDs Medical management starts with therapeutic doses of NSAIDs. These drug reduces inflammation
and pain but do not slow progression of RA. Another class of NSAIDs is COX-2 enzyme blockers have been
approved for treatments of RA. COX-2 medications block the enzyme involved in in inflammation (COX-2)
and are less likely to cause gastric irritation and ulceration than other NSAIDs; however, they are associated
with increased risk of cardiovascular disease.
DMARDs Disease-modifying antirheumatic drugs help slow or stop the progression of RA. The most
commono is methotrexate. It is the currently standard treatment of RA because of its success in preventing
both joint destruction and long term disability.
BIOLOGICS The newest treatment in for RA. Biologics are genetically engineered proteins that are
designed to inhibit specific components of the immune system that plays a vital role in inflammation.
Examples are etanercept (Enbrel), infliximab (Remicade), adalimumab (Humira), golimumab (Simponi),
which inhibit the function of TNF and anakira (Kineret).
CORTIOSTEROIDS Systemic corticosteroids decrease inflammation and other symptoms rapidly. However,
they do not prevent joint destruction, and rebound often follows the withdrawal of corticosteroids. They are
used while waiting for the DMARDs, and is prescribed for the shortest time necessary to minimize side
effects.
IMMUNOSUPPRESSIVE Prescribed because of their ability to affect the production of antibodies at the
cellular level. These include high dose methotrexate, cyclophosphamide (Cytoxan), azathioprine (Imuran), and
leflunomide (Arava). However, these drugs are more toxic. Thus, they are used only for patients in whom
treatment with DMARDs has failed. Cyclosporine (Neoral), an immunosuppressant, may be added to enhance
disease-modifying effect of methotrexate.

Nutrition

Client with RA frequently experience weight loss. Food selection should include the daily requirements from
the basic food groups, with emphasis on foods high in vitamins, protein, and iron for tissue building and repair.
Certain medications (oral corticosteroids) used in RA treatment stimulate the appetite and, when combined
with decreased activity, may lead to weight gain.

Surgery

Reconstructive surgery is indicated when pain cannot be relieved by conservative measures and the threat of
loss of independence is eminent. Surgical procedure include synovectomy (excision of synovial membrane),
tenorrhaphy (suturing of a tendon), arthrodesis (surgical fusion of joint), and athropaslty (surgical repair and
replacement of joint). Surgery is not performed during disease flares.
Nursing Management
The most common issues for the client includes pain, sleep disturbance, fatigue, altered mood, and
limited mobility. Client with newly diagnosed RA needs information about daily self-management to cope
having a chronic disease
Teaching Patients Self Care. Patient teaching enables the client to maintain as much independence as
possible and to take medications accurately and safely. Patient teaching focuses on the disorder itself, possible
changes related to disease, treatment, basic management and necessary adaptations in lifestyle, side effects of
medication, strategies to maintain independence and function, and patient safety in home. Pain, fatigue, and
depression can interfere with patients ability to learn and should be addressed before teaching is initiated.
Client who is elderly or frail, has RA that limits function significantly, and lives alone may need
referral for home care. Preventive skin care measures should be instruct because client can be at risk for
impaired skin integrity due to mobility problems. The nurse may administer injectable medications or teach the
client self-injection. The nurse also assesses the patients physical and psychosocial status, adequacy of

symptom management, and adherence to the management plan. The importance of attending follow-up
appointments is emphasized to the patient and family, and they should be reminded in participating other
health promotion activities and health screening.