Rheumatoid Arthritis 2 (Week 12) Flashcards
side effects of RA
fever rash lymph node enlargement spleen enlargement malaise Raynaud's
Rheumatoid nodules cause
excessive esudate escapes from the joint capsule and forms nodules in the region of the joint
where do rheumatoid nodules most commonly occur
dorsum of hands
Tx of RA
minimize inflammatory and immune processes
joint replacement
OT and PT goals for RA patients
- maintain joint ROM and muscle strength
- maintain independence in daily fxn
- modify activities to minimize stress and avoid continued joint destruction
best OT/PT interventions when not in a flare
heat application ROM exercise mild/moderate physical activity pool exercise (warm pool) splinting to prevent further contracture
best OT/PT interventions during a flare
cold application
rest affected joints
NO EXERCISE
vasculitis
inflammation of vascular endothelium
adenopathy
swollen lymph nodes
pathologies involved in RA
vasculitis neurologic dysfunction cardiopulmonary disease splenomegaly adenopathy
what percent of the population has RA
1%
what is the peak age for RA
7th decade
genetic predisposition for RA?
genetic predisposition that requires an environmental trigger
gender and RA
age 15-45: more women (6:1)
after 60: equal genders
other diseases associated with RA
smoking pulmonary disease epstein barr e. coli periodontal disease
what happens at the affected joint in RA
- chronic inflammation of synovial tissue
- inflammation of synovial tissue forms pannus, which invades cartilage and bone
- pannus destroys cartilage and bone
rheumatoid factors
autoantibodies in the IgM or IgG class
- present in blood of all RA patients
- bind to synovial membranes to form immune complexes
anticitrullinated protein (ACPA)
antibody produced by patients with RA
-typically present before symptoms are present
RA progression at synovial membrane and articular cartilage
- inflammation of the synovium causes movement of leukocytes into the tissue
- immune complexes promote inflammation
how do immune complexes promote inflammation at joint
- proinflammatory cytokines (TNF, IL-1, IL-6) promote release of more free radicals and hydrogen peroxide
- macrophages cause production of prostaglandins and other cytotoxins
what is used to treat RA
TNF inhibitors (biologic DMARDs)
janus kinase
hastens maturation and activity of leukocytes in the area
what is released at joint in RA
janus kinase histamines kinins leukocytes prostaglandins free radicals hydrogen peroxide
how does RA damage joint structure
- swelling of articular cartilage & synovial membrane
- swollen synovial membrane puts pressure on small vessels and other joint structures
- causes decreased BF to joint
- decreased BF causes hypoxia and acidosis (carbon dioxide levels increase)
what does acidosis cause in the joint
stimulate the release of hydrolytic enzymes from synovial cells
what do hydrolytic enzymes do
erode articular cartilage and inflame tendons and ligaments
-they break down just about anything
joints most commonly affected in RA
fingers feet wrists elbows ankles knees
areas less commonly affected in RA
shoulders hips cervical spine lungs heart kidney
