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Rheumatoid Arthritis

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Some key takeaways are that rheumatoid arthritis is a chronic inflammatory disease characterized by symmetrical joint involvement and persistent symmetric polyarthritis. It can be caused by genetic and environmental factors and has an autoimmune pathogenesis.

Rheumatoid arthritis is thought to be caused by a combination of genetic and environmental factors. Genetic susceptibility involves certain HLA genes, and environmental triggers may include infectious agents that activate the immune system.

Clinical manifestations of rheumatoid arthritis include morning stiffness, fatigue, joint warmth, swelling and pain. It can also involve extra-articular features such as inflammation of the salivary glands or lungs.

RHEUMATOID ARTHRITIS

What is RA?
A Chronic,
systemic inflammatory disease,
characterised by symmetrical
joint involvement which is
typically erosive/destructive.
hallmark feature: persistent
symmetric polyarthritis (synovitis)
Recap on the anatomy and physiology

Function of JOINTS:

• To allow articulation between two


or more bones and
• secondarily to permit movement
by contraction of opposing
muscles.
Etiology

•Unknown
• Genetic
• Autoimmune
Pathophysiology
Antigen –
Environmental agent, infectious agent

Genetic
Susceptibility Activates CD4 helper
HLA-DR4 T cells and probably
HLA-DQ B lymphocytes
HLA- DP
Cytokines

T cells stimulates
Activates
synovial macrophage
B lymphocytes
and fibroblast
Pathophysiology
T cells stimulates Activates B lymphocytes
synovial macrophage
and fibroblast
Formation of
rheumatoid
RANKL factor
Cytokines
Activates Formation of
osteoclast autoimmune complexes
Fibroblast and probable deposition
Chondrocytes in the joint
Synovial cells
Proliferation

Enzymes release Joint injury


(collagenase, streptomelysin, Pannus formation
elactase, PGE2 and matrix Joint destruction
metalloproteinases, others) Cartilage fibrosis
Ankylosis
INTERLEUKIN 1
IL-1 is a potent stimulator of synoviocytes,
chondrocytes and osteoblasts (Figure 1).
IL-1 is a proinflammatory cytokine that amplifies
and perpetuates the disease process in RA
Clinical Manifestations
1. arthritis
Associated with
•low fever
•Fatigue
•Morning stiffness
•Joint soft, warm to
touch
Clinical Manifestations
2. extra-articular features
Clinical Manifestations
3. Associated syndromes
(possible complications)
(a) Sjögren’s syndrome-salivary gland
inflammation and keratoconjunctivitis
(b) Felty’s syndrome-profound neutropenia,
thrombocytopenia and splenomegaly
(C) Pulmonary involvement-(pleuritis, interstitial
pneumonitis, alveolitis and intrapulmonary
rheumatoid nodules)
(d) Cardiac involvement-pericarditis
ns
Diagnnostic criteria
1. Morning stiffness lasting more than

1 hour
2. Arthritis of 3 or more joint areas.
3. Arthritis of the hand joints
4. Symetric arthritis
5. Rheumatoid nodules over extensor
surface or bony prominences.
6. Serum rheumatoid factor.
7. Radiologic changes.
Types of JIA

• oligoarticular JIA
•Polyarticular JIA
•Systemic JIA  
Nursing Diagnosis:

1. Acute Pain r/t inflammation & swelling


2. Fatigue r/t increased metabolic rate
3. Impaired physical mobility r/t decreased
range of motion
4. Disturbed body image r/t physical &
psychological changes
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