MIDTERMS: Seronegative Spondyloarthropathy & Systemic Lupus Flashcards
Q: What is seronegative spondyloarthropathy?
A: A group of diseases affecting joints, spine, and entheses, occurring without rheumatoid factor (RF).
Q: What genetic marker is associated with seronegative spondyloarthropathy?
A: HLA-B27.
Q: What are the key features of seronegative spondyloarthropathy?
No RF antibodies.
Asymmetric arthritis.
Enthesitis (inflammation where tendons/ligaments attach to bones).
Inflammatory back pain.
Q: What diseases are included in seronegative spondyloarthropathy?
Ankylosing Spondylitis (AS)
Reactive Arthritis (ReA)
Psoriatic Arthritis (PsA)
Inflammatory Bowel Disease (IBD)-associated arthritis
Juvenile Spondyloarthropathy
Q: What is ankylosing spondylitis (AS)?
A: A chronic inflammatory disease affecting the axial skeleton (spine and sacroiliac joints).
Q: What is the most common initial symptom of AS?
A: Inflammatory back pain, especially in the lower back and buttocks.
Q: What is the hallmark radiographic feature of AS?
A: Sacroiliitis – bilateral sacroiliac joint inflammation with erosion and fusion.
Q: What is systemic lupus erythematosus (SLE)?
A: A chronic autoimmune disease where the immune system attacks multiple organs due to autoantibody production.
Q: What are the extra-articular features of AS?
Uveitis (eye inflammation).
Inflammatory bowel disease (IBD).
Aortic insufficiency (heart involvement).
Q: How is AS managed?
NSAIDs (first-line).
TNF inhibitors (if severe) – e.g., Infliximab, Etanercept.
Physical therapy to maintain spinal mobility.
Q: What infections are commonly associated with reactive arthritis?
Chlamydia trachomatis (genitourinary).
Salmonella, Shigella, Yersinia, Campylobacter (gastrointestinal).
Q: What is reactive arthritis?
A: An inflammatory arthritis that occurs after an infection (commonly GI or genitourinary infections).
Q: What are the clinical features of psoriatic arthritis?
Asymmetric arthritis.
Dactylitis (sausage fingers/toes).
Nail pitting & onycholysis.
Enthesitis (Achilles tendon, plantar fascia).
Q: What does “seronegative” in seronegative spondyloarthropathy mean?
A: The absence of rheumatoid factor (RF) and anti-CCP antibodies.
Q: What is the classic triad of reactive arthritis?
A: Arthritis, conjunctivitis, urethritis (“Can’t see, can’t pee, can’t climb a tree”).
Q: How is reactive arthritis treated?
NSAIDs (first-line).
Antibiotics (if infection is still present).
DMARDs (Methotrexate, Sulfasalazine) for persistent cases.
Q: What is psoriatic arthritis?
A: A type of inflammatory arthritis associated with psoriasis.
Q: How is psoriatic arthritis treated?
NSAIDs for mild cases.
DMARDs (Methotrexate, Sulfasalazine, Leflunomide) for moderate disease.
Biologics (TNF inhibitors, IL-17 inhibitors) for severe cases.
Q: What is the first symptom of ankylosing spondylitis?
A: Inflammatory back pain that improves with activity.
Q: What is the hallmark radiologic feature of AS?
A: Bamboo spine (vertebral fusion on X-ray).
Q: What are the four major seronegative spondyloarthropathies?
Ankylosing Spondylitis (AS).
Reactive Arthritis (ReA).
Psoriatic Arthritis (PsA).
Inflammatory Bowel Disease (IBD)-associated arthritis.
Q: What test is used to assess spinal mobility in AS?
A: Schober’s test.
Q: What is the primary treatment for AS?
A: NSAIDs (first-line), followed by TNF inhibitors if severe.
Q: What triggers reactive arthritis?
A: Post-infectious response, commonly after Chlamydia (GU infection) or Salmonella/Shigella/Yersinia/Campylobacter (GI infection).
Q: What is a key clinical sign of psoriatic arthritis?
A: Dactylitis (sausage fingers/toes).
Q: What are the five patterns of psoriatic arthritis?
Asymmetric oligoarthritis.
Symmetric polyarthritis (RA-like).
DIP joint arthritis.
Arthritis mutilans (severe bone resorption).
Spondylitis with sacroiliitis.
Q: What are the major risk factors for SLE?
Gender: 80–90% occur in women of childbearing age.
Ethnicity: More common in African, Native American, Hispanic, and Asian populations.
Triggers: UV light, infections, hormonal changes, and certain drugs.
Q: What is the main mechanism of SLE pathophysiology?
A: Overactive immune response leads to immune complex formation and tissue inflammation.
Q: What genetic factors increase susceptibility to SLE?
A: HLA-DR2, HLA-DR3.
Q: What are the common skin manifestations of SLE?
Malar (butterfly) rash across cheeks and nose.
Discoid lupus (scarring plaques).
Photosensitivity (rash worsens with sun exposure).
Q: What are the common musculoskeletal symptoms of SLE?
Polyarthritis (non-erosive, affects small joints).
Osteonecrosis (hip & shoulder, linked to steroid use).
Myositis (muscle inflammation and weakness).
Q: What are the renal complications of SLE?
A: Lupus nephritis – inflammation of the kidneys, causing proteinuria, hematuria, and hypertension.
Q: How is SLE diagnosed?
A: Antinuclear Antibody (ANA) test (highly sensitive).
Other markers: Anti-dsDNA, Anti-Smith (Anti-Sm), Anti-phospholipid antibodies.
Q: What are the main treatments for SLE?
NSAIDs – Pain relief for joint symptoms.
Corticosteroids – Reduce inflammation.
Hydroxychloroquine – Used for skin/joint manifestations.
Immunosuppressants (Methotrexate, Azathioprine, Mycophenolate) – Used for severe cases.
Q: What is the hallmark feature of SLE?
A: Autoantibody production leading to immune complex deposition and multi-organ inflammation.
Q: What autoantibodies are most specific for SLE?
A: Anti-dsDNA and Anti-Smith (Anti-Sm).
Q: What autoantibody is sensitive but not specific for SLE?
A: Antinuclear Antibody (ANA).
Q: What are the common systemic symptoms of SLE?
Fatigue
Fever
Weight loss
Lymphadenopathy
Q: What are the main dermatologic manifestations of SLE?
Malar (butterfly) rash – spares the nasolabial folds.
Discoid rash – scaly, atrophic plaques.
Photosensitivity – rash triggered by UV exposure.
Q: What are the common cardiovascular complications in SLE?
Libman-Sacks endocarditis (non-bacterial vegetations on heart valves).
Pericarditis.
Increased risk of atherosclerosis.
Q: What is the drug-induced lupus triad?
Arthralgia/myalgia.
Serositis (pleuritis/pericarditis).
Positive Anti-histone antibodies.
Q: What drugs are commonly associated with drug-induced lupus?
Hydralazine.
Isoniazid (INH).
Procainamide.
Q: What is the first-line treatment for mild SLE?
Hydroxychloroquine
