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RHEUMATOI

D ARTHRITIS
Rheumatoid Arthritis is an autoimmune disease of
unknown origin that affects 1% of the population.

Rheumatoid arthritis (RA) is a chronic, systematic


autoimmune disorder that causes the immune system
to attack the joints, where it causes inflammation
(arthritis) and destruction. It can also damage some
organs, such as the lungs and skin. It can be a disabling
and painful condition, which can lead to substantial loss
of functioning and mobility. Rheumatoid arthritis is an
inflammatory form of arthritis that causes joint pain
and damage.
CAUSES
Autoimmune Factor: occurs when white blood cells – whose
usual job is to attack unwanted invaders, such as bacteria and
viruses – move from your bloodstream into the membranes that
surround your joints (synovium). The blood cells appear to play a
role in causing the synovium to become inflamed. The
inflammation causes the release of proteins that, over months
or years cause the synovium to thicken. The proteins can also
damage the cartilage, bone, tendons and ligaments near your
joint. Gradually, the joints loses its shape and alignment.
Eventually, it may be destroyed.
Genetic (inherited) factors: scientists have discovered that
certain genes known to play a role in the immune system are
associated with a tendency to develop rheumatoid arthritis.
Some people with rheumatoid arthritis do not have these
particular genes; still others have these genes but never develop
the disease.
 Environmental factors: Many scientists think that
something must occur to trigger the disease process
in people whose genetic makeup makes them
susceptible to rheumatoid arthritis.
 Lifestyle choices
 Hormonal factor: Some scientists also think that a
variety of hormonal factors may be involved. Women
are more likely to develop rheumatoid arthritis than
men, pregnancy may improve the disease, and the
disease may flare after a pregnancy. Breastfeeding
may aggravate the disease.
 
Predisposing Factor Precipitating Factor
Gender (female) Diet
Age (20-50 y/o) Lifestyle
Occupation

Presentation of Swelling in small


antigen T cells joints, associated
with pain, stiffness,
and fatigue

T and B cell proliferation, Warm, swollen,


Angiogenesis in synovial effusions, pain, and
lining decreased motion
with possible
rheumatoid
Neutrophil Synovitis. Early pannus nodules
accumulation in invasion. Chondrocyte Increase in severity
synovial fluid. Cell invasion, Degredation of physical sign and
proliferation. No of cartilage by symptoms
cartilage invasion proteinase
Subchondral bonde erosin, Joint instability,
pannus invasion of the contractures,
cartilage. Chondrocyte decreased ROM,
proliferation. Laxity of systemic
ligaments Rheumatoid Arthritis complication.
Clinical Manifestation

Joint Pain

Swelling

Warmth

Erythema

Lack of function

Join stiffness in the morning


In early stage of disease, even before bony changes occur,
limitation in function can occur when there is active
inflammation of the joints., swollen, and painful are not easily
moved. Immobilization for extended periods can lead to
contractures, creating soft tissue deformity.

Deformity of the hands and feet are common in RA. The


deformity may caused by mis alignment resulting from
swelling, progressive joint destruction or the subcluxation
(partial dislocation) that occurs when one boneslips over
another and eliminates the joint space.
Most common are fever, weight loss, fatigue, anemia, lymph
nodes enlargement, and raynaud’s phenomenon (cold and
stress-induced vasospasm causing episodes of digital blanking
or cyanosis).
ASSESSMENT
 The history and physical examination address manifestation such as
bilateral and symmetric stiffness, tenderness, swelling and
temperature changes in the joints.
 The patient is also assessed for extra-articular changes; these often
include weight loss, sensory changes lymph node enlargement, and
fatigue.

DIAGNOSTIC TEST
 The ESR is significantly elevated in RA.
 The Red Blood Cell count and C4 complement component are
decreased.
 C-reactive protein and anti-nuclear antibody (ANA) test result may
also be positive
 Arthrocentesis shows synovial fluid that is cloudy, milky, or dark
yellow and contains numerous inflammatory components
Medical Management
 Early Rheumatoid Arthritis

 Medical Management begins with therapeutic doses of


salicylates or NSAIDs. When used in full therapeutic dosages,
these medications provide both anti-inflammatory and analgesic
effects.
 Cyclo-oxygenase is an enzyme that is involved the anti-
inflammatory process. However.they are associated
withincreased risk of cardiovascular disease and must be used
with caution.
 Treatment with the DMARDs (antimalarials, gold, penicillamine,
or sulfasalazine) begin with 3 months of disease onset .
 If symptoms are aggressive methotrexate mau be
considered because of its success in preventing both joint
destruction and long term disability.

 Etanercept,infliximab, adalimumab and golimumab


inhibit the function of TNF-alpha, a key cytokine known to
play a role in the disease process in RA, whereas anakinra
inhibit the function of inter-leukine-1.

 Another analgesia may be prescribed for periods of


extreme pain. Opiod analgesic agents are
avoidedbaceause of the potential for continuing need for
pain relief.
NON-PHARMACOLOGIC PAIN
MANAGEMENT TECHNIQUES:

 Relaxation techniques
 Heat and cold application

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