Pathophysiology of Rheumatoid Arthritis Exam 1 Flashcards
1
Q
What is the prevalence of RA?
A
1% of U.S. population but all populations affected
2
Q
Who is susceptible to getting RA?
A
- More common in women
* Most common age of onset: 40-60 y
3
Q
relate mortality to RA
A
mortality is increased; correlates with severity as measured by number of joints involved, functional status, etc.
4
Q
Etiologies of RA
A
- Genetic predisposition: HLA-DR4
- Unidentified etiologic agent: environmental such as virus or bacteria, periodontal disease, or smoking which initiates immune response
5
Q
Pathogenesis of RA
A
- Inflammatory response with progressive activation of many types of cells
- Initial immune response followed by lymphocyte proliferation
- Inflammation promoted by release of pro-inflammatory cytokines
- Synovial proliferation follows
- Neutrophils accumulate in synovial fluid, with activation of chondrocytes and initiation of enzyme degradation of cartilage
- Invasion of cartilage
6
Q
Remission criteria
A
Scoring ≤ 1 on all of the following
- Tender joint count
- Swollen joint count
- CRP (in mg/dL)
- Patient global assessment (0-10 scale)
7
Q
ACR criteria for functional classes
A
- Class I: Able to perform usual activities (self-sufficient)
- Class II: Able to perform usual self-care and vocational activities, but limited in avocational activities
- Class III: Able to perform usual self-care, but limited in vocational and avocational activities
- Class IV: Limited in ability to perform usual self-care, vocational, and avocational activities
8
Q
RA joint changes
A
- Early: active inflammation with soft-tissue swelling and effusion
- As inflammation continues, chronic damage to supporting soft-tissue structures leads to joint deformity including:
• Swan-neck deformity (hyperextension at PIP, flexion at DIP)
• Boutonniere deformity (flexion at PIP, extension at DIP)
• Ulnar deviation (at MCPs)
• Subluxation (partial dislocation) (MCPs and others)
9
Q
Joint involvement
A
- Wrists are very commonly involved, in contrast to OA
- Any synovial joint may be involved
- Low back pain is usually not caused by RA, but cervical spine involvement is common
- In RA, involvement of PIPs and MCPs is more frequent than involvement of DIPs.
10
Q
Extra-articular manifestations
A
- Systemic symptoms (fever, malaise, weakness, myalgias, fatigue)
- Rheumatoid nodules
- Pleuro-pericardial disease (interstitial lung disease, pleural effusions, lung nodules, pericarditis)
- Eye (involvement of the sclera [episcleritis, scleritis])
- Sjögren syndrome (dry eyes and mouth)
- Hematologic
- Vasculitis
- Cardiovascular disease
11
Q
Disease course of RA (according to handout)
A
Most have chronic inflammation with relative exacerbations and remissions, but severity may vary
12
Q
monitoring of RA disease activity
A
- Erythrocyte sedimentation rate (ESR) is usually elevated in RA, reflecting acute phase response.
- C-reactive protein (CRP) also reflects acute phase response (inflammation) and disease activity (does not always agree with ESR)
- Serum viscosity and fibrinogen are other factors that rise in inflammation
- Albumin falls with chronic inflammation; globulins are often high in RA
- Platelets rise with inflammatory state, especially in juvenile idiopathic arthritis
- Anemia of chronic disease is very common in active RA
13
Q
Comparing RA and OA
A
- Average age of onset for OA is older
- RA is typically symmetrical in distribution of involvement
- Frequency of involvement at specific sites (MCPs, PIPs, wrists in RA; DIPs, PIPs, 1st CMC in OA)
- Duration and severity of morning stiffness (RA > OA)
- Prominence of joint inflammation in RA; not in OA
- Systemic or extra-articular symptoms in RA; not in OA
- Bone erosions in RA; bony enlargement (osteophytes) in OA
- RA with symmetrical joint space narrowing on x-ray vs. OA with sclerosis, osteophytes, and irregular narrowing.
- RA with RF & anti-CCP, elevated ESR & CRP, other signs of chronic inflammatory condition; OA – no consistent lab findings
