Rheumatoid Arthritis Flashcards
What is rheumatoid arthritis (RA)?
A chronic autoimmune inflammatory disease primarily affecting synovial joints, leading to progressive joint damage and systemic complications.
What is the hallmark feature of RA?
Symmetrical polyarthritis, typically involving small joints (e.g., hands, wrists, feet).
Who is most commonly affected by RA?
Women (3:1 female-to-male ratio).
Peak onset: 30–50 years of age.
What are the key genetic risk factors for RA?
HLA-DR4 and HLA-DR1 alleles.
Polymorphisms in PTPN22 and other immune-regulatory genes.
What environmental factors are associated with RA?
Smoking: Strongest modifiable risk factor.
Periodontal infections (e.g., Porphyromonas gingivalis).
Silica exposure.
What is the key immunologic mechanism in RA?
Autoimmune activation leads to synovial inflammation, pannus formation, and joint destruction.
What role do autoantibodies play in RA?
Rheumatoid factor (RF): Autoantibody against IgG Fc.
Anti-cyclic citrullinated peptide (anti-CCP) antibodies: Specific for RA, targeting citrullinated proteins.
What inflammatory cytokines are involved in RA?
Tumor necrosis factor-alpha (TNF-α).
Interleukin-1 (IL-1).
Interleukin-6 (IL-6).
What are the hallmark joint features of RA?
Symmetrical joint involvement.
Morning stiffness lasting >1 hour.
Swelling, warmth, and tenderness of affected joints.
What joints are typically affected early in RA?
Small joints: MCPs, PIPs, wrists, MTPs.
Sparing of DIP joints (distinguishes RA from osteoarthritis).
What are common deformities in advanced RA?
Swan neck deformity: Hyperextension of PIP, flexion of DIP.
Boutonnière deformity: Flexion of PIP, hyperextension of DIP.
Ulnar deviation of the fingers.
What are common extra-articular features of RA?
Rheumatoid nodules (subcutaneous, over extensor surfaces).
Lung: Interstitial lung disease, pleuritis, pulmonary nodules.
Cardiovascular: Increased risk of atherosclerosis, pericarditis.
Hematologic: Anemia of chronic disease, Felty syndrome (RA, splenomegaly, neutropenia).
Neurologic: Peripheral neuropathy, atlantoaxial subluxation.
Eyes: Scleritis, episcleritis, keratoconjunctivitis sicca (dry eye).
How is RA diagnosed?
Based on clinical, serologic, and imaging criteria (ACR/EULAR classification).
What laboratory findings support a diagnosis of RA?
Positive RF (present in ~70–80% of cases).
Positive anti-CCP antibodies (high specificity).
Elevated ESR and CRP (markers of inflammation).
What imaging findings are characteristic of RA?
Early: Soft tissue swelling, periarticular osteopenia.
Late: Joint erosions, subluxation, and joint space narrowing.
What is the cornerstone of RA treatment?
Disease-modifying antirheumatic drugs (DMARDs).
What is the first-line DMARD for RA?
Methotrexate, used as monotherapy or in combination.
What are other conventional DMARDs?
Leflunomide.
Sulfasalazine.
Hydroxychloroquine.
What are biologic therapies used in RA?
TNF inhibitors: Adalimumab, infliximab, etanercept.
IL-6 inhibitors: Tocilizumab.
Costimulation blockers: Abatacept.
B-cell depletion: Rituximab.
What role do corticosteroids play in RA?
Low-dose corticosteroids are used for short-term symptom relief during flares or while awaiting DMARD efficacy.
What factors indicate a poor prognosis in RA?
Early joint erosions.
High levels of RF or anti-CCP antibodies.
Extra-articular involvement.
High disease activity at diagnosis.
How does osteoarthritis differ from RA?
Joint involvement: OA affects weight-bearing joints (knees, hips) and DIP joints; RA typically involves MCPs, PIPs, and wrists.
Symmetry: OA is often asymmetric, while RA is symmetrical.
Morning stiffness: OA stiffness lasts <30 minutes; RA stiffness lasts >1 hour.
Inflammatory signs: OA has minimal inflammation; RA involves warmth, swelling, and tenderness.
Radiographic findings:
- OA: Joint space narrowing, subchondral sclerosis, osteophytes.
- RA: Periarticular osteopenia, erosions.
Serology: Negative RF and anti-CCP in OA.
How is psoriatic arthritis distinguished from RA?
Skin findings: PsA is associated with psoriatic plaques or nail pitting, absent in RA.
Joint pattern: PsA can involve DIP joints and is often asymmetric; RA spares DIP joints and is symmetrical.
Enthesitis: PsA often causes inflammation where tendons attach to bone (e.g., Achilles tendon); uncommon in RA.
Radiographic findings: PsA shows “pencil-in-cup” deformities and periostitis; RA shows joint erosions and periarticular osteopenia.
Serology: RF and anti-CCP are typically negative in PsA.
How does SLE differ from RA?
Systemic features: SLE has a wide range of systemic symptoms (rash, renal, hematologic, and CNS involvement), while RA predominantly affects joints.
Joint involvement: SLE causes non-erosive, migratory arthritis; RA causes erosive arthritis.
Skin findings: SLE has a malar rash, discoid rash, and photosensitivity, absent in RA.
Serology:
- SLE: Positive ANA, anti-dsDNA, anti-Smith antibodies.
- RA: Positive RF and anti-CCP.
Radiographic findings: No erosions in SLE; erosions are typical in RA.
How is reactive arthritis differentiated from RA?
Preceding infection: ReA follows infections (e.g., gastrointestinal or genitourinary infections); RA has no such trigger.
Joint pattern: ReA is typically asymmetric and affects large joints, especially in the lower extremities; RA is symmetrical and affects small joints.
Systemic symptoms: ReA can involve uveitis, conjunctivitis, and urethritis (“can’t see, can’t pee, can’t climb a tree”), which are not features of RA.
Serology: Negative RF and anti-CCP in ReA.
HLA-B27 association: Strongly associated with ReA but not with RA.
