ASUHAN KEPERAWATAN
Rheumatoid Arthritis:
MARIDI M. DIRDJO
Rheumatoid Arthritis
• RA has an incredibly high disease burden
and cost to society
• Drastic affect on quality of life
• Increased disability (80% disabled after 20
years of disease)
• Patients with RA have shorter life
expectancies
• It is important to initiate therapy early so
as to halt/slow disease progression
What is Rheumatoid Arthritis?
A chronic disease characterized by the
inflammation of the lining of the joints, which is
called the synovium.
Affects 2.1 million Americans between the ages of
20 and 50, but also affects young children and
adults over 50
More common in women than men.
Known as an autoimmune disease because the
body’s immune system attacks the joint lining.
Autoimmune and Inflammatory Disorders:
Rheumatoid Arthritis
Chronic systemic, inflammatory disease
characterized by recurrent inflammation of
connective tissue, primarily of joints
(diarthroidal) and related structures.
Pathogenesis
• Exact mechanism unknown
• Most likely related to acute and chronic
inflammation in the synovium in addition to
a proliferate and destructive process of
joint tissues
Pathophysiology Rheumatoid
Arthritis
• Normal antibodies (immunoglobulins)
become autoantibodies and attack host
tissues (RF)
– Neutrophils, T cells synovial fluid cells acitavted;
– Cystokines, interleukin-1 and TNR (tumor necrosing factor)
alpha; chrondroytes attack cartilage;
– Synovium digests cartilage; inflammatory molecules released
containing interleukin-1 and TNF alpha
Pathophysiology: Rheumatoid
Arthritis
• Pathophysiology
• IgG/RF (HLA)= antigen-antibody
complex
– Precipitates in synovial fluid
– Inflammatory response
• Cartilage connective tissue primarily
affected!
What is the cause of this
disease?
The exact cause of RA is unknown.
Suspected causes are:
Bacterial Infection
Genetic Marker
Stress
Viral Infection
Symptoms of RA Patients
• Fatigue.
• Stiffness, especially in early morning and after
sitting a long period of time.
• Low Grade Fever, Weakness.
• Muscle pain and pain with prolonged sitting.
• Symetrical, affects joints on both sides of the
body.
• Rheumatoid nodules.
• Deformity of your joints over time.
Rheumatoid arthritis: assessment:
manifestations and complications
• Fatigue,
weakness,
pain
• Joint
deformity
• Rheumatic
nodules
• Multisystem
involvement
Juvenile Rheumatoid Arthritis
• Causes joint inflammation and stiffness for
more than six weeks in a child of 16 years
of age or less.
• There are three types, classified by the
number of joints involved and symptoms.
• Pauciarticular, the most common, four
joints or fewer are affected.
JRA
• Polyarticular, where five or more joints are
affected.
• Systemic, besides joint swelling, a fever and
light skin rash is present.
• Symptoms are similar to adults, joint swelling,
pain, and stiffness in the morning or after a nap.
It commonly affects the knees and joints in the
hands and feet
How does the immune system
play a role in this disease
• In RA, for some unknown reason, the immune
system considers its own joint tissues foreign.
• White blood cells that normally protect the body,
migrate to the joint cavity.
• Synovium becomes inflammed and engorged with
fluid, causing synovitis.
• Lymphocytes, Macrophages, continue to enter the
joint cavity and multiply, differentiate, and release
inflammatory mediators, cytokines, leukotrienes,
and prostaglandins.
• Within weeks the synovium becomes
thickened.
• The mass of synovial tissue that spreads
over the top of cartlidge in a rheumatoid
joint is called a pannus, made of white
blood cells: macrophages, B&T Cells,
neutrophils, plasma cells, NK cells, and T
Helper cells.
• These cells produce the Rheumatoid
Factor, prostaglandins, cytokines and
other mediators.
• Over time, the chemicals from the cells
damage cartilage, ligaments, tendons, and
bone.
Hill, J., & Hale, C (2004) British Journal of Nursing, Vol 13, No 14. 852-857
Diagnosis Of RA
• Clinical History
• Physical Exams
• Specific Lab Tests
CBC
ESR
CRP
RA Factor
Anti CCP
• Imaging Studies
X-Ray
MRI
Cat Scan
Bone Scan
Conventional Methods of
Treatment
• Nonsteroidal Anti Inflammatory Drugs (NSAIDs)
– Aspirin, Ibuprofen, COX-2 inhibitor.
• Corticosteroids – Cortisone
• Disease Modifying Antirheumatic Drugs
(DMARDs) – Methotrexate, Injectable Gold,
Hydroxychloroquine.
• Biologic Response Modifiers – Enbrel,
Remicade, Humira.
Alternative Methods of
Treatment
• Diet
• Exercise
• Acupuncture
• Herbal Medicines
• Massage
• Stress Reduction Techniques – prayer,
meditation, hypnosis, yoga, tai-chi.
The Bottom Line!!
Treatment Options
• Methotrexate has been one of the
mainstays of RA treatment
– Action: Inhibits dihydrofolate reductase
• Over the past few years newer biologic
disease modifying anti-rheumatic drugs
have been developed
• These drugs target select aspects of the
immune response so as to decrease
inflammation
Etanercept
• Recombinant fusion protein of the TNF (tumor
necrosis factor) receptor that is solubilized by
linking to the Fc portion of human IgG1
• Inhibits TNF: cytokine produced primarily by
macrophages
• Administered by subcutaneous injection twice
weekly
• Extremely expensive
Mechanism of Etanercept
PC RF
Autoantibodies
B B PC
Activates
Activates Inflammation
T Joint damage
T T
T T FLS FLS
APC/DC
T
Activates
X Etanercept
TNF
MΦ MΦ
Clinical Question
• Is Etanercept superior to MTX when used
as a monotherapy for early RA?
• Is combination therapy consisting of both
MTX and Etanercept superior to either
MTX or Etanercept alone?
ACR Response Criteria
≥ 20% / 50% / 70% Improvement in:
• Number of swollen joints (SJC)
• Number of tender joints (TJC)
• Improvement of at least three of the following:
• Patient Global Assessment
• Physician Global Assessment
• Patient Pain Scale
• Health Assessment Questionnaire (HAQ)
• ESR or CRP
Felson DT et al. Arthritis Rheum. 1993; 41: 1564-1570
ERA (Early rheumatoid arthritis trial)
Tempo Trial
MTX
Klareskog et al. Lancet. 2004;363:675
COMET – combo vs monotherapy
ACR Score
Methotrexate
100
86 Etanercept +
Methotrexate
Proportion of patients (%)
80 71
67
60
49 48
40
28
20
0
AR20 ACR50 ACR70
Emery et al. Lancet 2008; 372: 375–82
Negatives / Side effects
• Entanercept
– Injection site infections
– Good safety profile for the most part – rare events
resulting from immunosuppression (TB, opportunistic
infections, URIs), slightly increased risk of lymphoma
and CHF, drug induced lupus
• MTX
– Pneumonitis,hepatic toxicity, anemia,
thrombocytopenia, leukopenia, slightly increased risk
of lymphoma, alopecia, mouth ulcers, N/V
- Frequent laboratory testing needed. (3-6 times a
year) Requires folic acid supplementation.
Diagnosis Keperawatan
• Impaired physical mobility related tojoint
pain, stiffness, and deformity
• Chronic pain related to joint
inflammation, misuse of joints, and
ineffective pain and/or comfort measures
• Disturbed body image related tochronic
disease activity, long-term treatment,
deformities, stiffness, and inability to
perform usual activities
References
Arthritis Foundation. “Disease Center.” Arthritis Foundation. 2004. 24 Aug. 2005.
< [Link]
Arthritis Foundation. Good Living with Rheumatoid Arthritis. Atlanta: Arthritis Foundation, 2004.
Lahita, Robert G. M.D. Rheumatoid Arthritis – Everything You Need to Know. New York:
Avery, 2001
Mayo Clinic. “Rheumatoid Arthritis.” Mayo [Link]. Mayo Foundation for Medical
Education and Research. 8 April. 2005. 10 Oct. 2005
[Link]
National Institute of Arthritis and Musculoskeletal and Skin Diseases. “Questions and Answers
About Juvenile Rheumatoid Arthritis.” National Institute of Health. 2001 July. 10 Oct. 2005.
<[Link]
Oxford Journals. “Alfred Baring Garrod.” Heberden Historical Series. British Society for
Rheumatology. 2001. 28 Oct. 2005.
<[Link]
Parham, Peter. The Immune System. New York: Garland Science Publishing, 2005.
Shlotzhauer, Tammi L. M.D. and James McGuire M.D. Living with Rheumatoid Arthritis.
Baltimore: John Hopkins University Press, 2003.
