1. Genetic environmental and
immunologic factors

2. Activation of T cell mediated immune response (CD4+ cells, interleukin, and tissue necrosis factor)

3. RF antigen/ IgG interaction

4. Immune Complexes deposited into joint space and osteoclasts are activated

5. B and T lymphocytes to stimulate the inflammatory response

6. Angiogenesis in synovium

7. Synovial proliferation causing thickening and fluid accumulation

8. Pannus formation of granulation tissue that is composed of inflammatory cells that erodes the articular tissue.

Acute inflammatory symptoms

Weakness

Fatigue

Chronic Inflammatory Symptoms

Rheumatoid Vascularitis

Mediator:
Release of
TNF, IL-1

Disease onset: occurs at any age,
peak incidence between 50-75 years
old. Women are affected more frequently than males

Cigarette smoking is the strongest risk factor for the development of RA

70-80% of people who have RA have a RF factor which is an antibody that reacts with a fragment of IgG to form immune complexes

Presence of Anti-cyclic citrulline peptide antibodies

Neutrophils and macrophages phagocytize immune complexes releasing lysosomal enzymes that destroys articular cartilage

9. Destruction and calcification of articular
cartilage and underlying bone

Localized joint inflammation

Permanent hand deformity

Swan's neck

Boutonniere

joint pain

Joint swelling

Joint redness

Morning Stiffness for more than 30 min

Chronic Systemic Symptoms from calcification of articular cartilage

Rheumatoid nodules

RHEUMATOID ARTHRITIS CONCEPT MAP

Nursing Intervention: Educate patient on using heat and cold therapy to relieve inflammation and pain

Nursing Intervention: Encourage patient to engage in physical activity to slow down joint damage

Other joints including proximal interphalangeal joints, shoulder, elbows, hips, knees and ankles

Pharmacologicals

DMARDS

NSAIDS

Corticosteroids