Rheumatoid Arthritis Flashcards

1
Q

What is rheumatoid arthritis (RA)?

A

A chronic autoimmune inflammatory disease primarily affecting synovial joints, leading to progressive joint damage and systemic complications.

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2
Q

What is the hallmark feature of RA?

A

Symmetrical polyarthritis, typically involving small joints (e.g., hands, wrists, feet).

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3
Q

Who is most commonly affected by RA?

A

Women (3:1 female-to-male ratio).

Peak onset: 30–50 years of age.

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4
Q

What are the key genetic risk factors for RA?

A

HLA-DR4 and HLA-DR1 alleles.

Polymorphisms in PTPN22 and other immune-regulatory genes.

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5
Q

What environmental factors are associated with RA?

A

Smoking: Strongest modifiable risk factor.

Periodontal infections (e.g., Porphyromonas gingivalis).

Silica exposure.

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6
Q

What is the key immunologic mechanism in RA?

A

Autoimmune activation leads to synovial inflammation, pannus formation, and joint destruction.

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7
Q

What role do autoantibodies play in RA?

A

Rheumatoid factor (RF): Autoantibody against IgG Fc.

Anti-cyclic citrullinated peptide (anti-CCP) antibodies: Specific for RA, targeting citrullinated proteins.

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8
Q

What inflammatory cytokines are involved in RA?

A

Tumor necrosis factor-alpha (TNF-α).

Interleukin-1 (IL-1).

Interleukin-6 (IL-6).

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9
Q

What are the hallmark joint features of RA?

A

Symmetrical joint involvement.

Morning stiffness lasting >1 hour.

Swelling, warmth, and tenderness of affected joints.

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10
Q

What joints are typically affected early in RA?

A

Small joints: MCPs, PIPs, wrists, MTPs.

Sparing of DIP joints (distinguishes RA from osteoarthritis).

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11
Q

What are common deformities in advanced RA?

A

Swan neck deformity: Hyperextension of PIP, flexion of DIP.

Boutonnière deformity: Flexion of PIP, hyperextension of DIP.

Ulnar deviation of the fingers.

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12
Q

What are common extra-articular features of RA?

A

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).

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13
Q

How is RA diagnosed?

A

Based on clinical, serologic, and imaging criteria (ACR/EULAR classification).

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14
Q

What laboratory findings support a diagnosis of RA?

A

Positive RF (present in ~70–80% of cases).

Positive anti-CCP antibodies (high specificity).

Elevated ESR and CRP (markers of inflammation).

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15
Q

What imaging findings are characteristic of RA?

A

Early: Soft tissue swelling, periarticular osteopenia.

Late: Joint erosions, subluxation, and joint space narrowing.

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16
Q

What is the cornerstone of RA treatment?

A

Disease-modifying antirheumatic drugs (DMARDs).

17
Q

What is the first-line DMARD for RA?

A

Methotrexate, used as monotherapy or in combination.

18
Q

What are other conventional DMARDs?

A

Leflunomide.

Sulfasalazine.

Hydroxychloroquine.

19
Q

What are biologic therapies used in RA?

A

TNF inhibitors: Adalimumab, infliximab, etanercept.

IL-6 inhibitors: Tocilizumab.

Costimulation blockers: Abatacept.

B-cell depletion: Rituximab.

20
Q

What role do corticosteroids play in RA?

A

Low-dose corticosteroids are used for short-term symptom relief during flares or while awaiting DMARD efficacy.

21
Q

What factors indicate a poor prognosis in RA?

A

Early joint erosions.

High levels of RF or anti-CCP antibodies.

Extra-articular involvement.

High disease activity at diagnosis.

22
Q

How does osteoarthritis differ from RA?

A

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.

23
Q

How is psoriatic arthritis distinguished from RA?

A

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.

24
Q

How does SLE differ from RA?

A

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.

25
Q

How is reactive arthritis differentiated from RA?

A

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.