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Quizzes > Health & Medicine > Diseases & Conditions

Test Your Rheumatoid Arthritis Knowledge Now

Think you can ace this RA quiz? Dive into our Have I Got Rheumatoid Arthritis Quiz now!

Difficulty: Moderate
2-5mins
Learning OutcomesCheat Sheet
Paper art illustration for rheumatoid arthritis quiz shows joint icons, pills and quiz title on coral background.

Use this Rheumatoid Arthritis Quiz to check how well you understand key symptoms, causes, early signs, and treatment choices. You'll spot gaps fast, learn a few helpful facts, and if you're unsure about your own joints, try a quick self-check. Then play again to improve.

What best describes rheumatoid arthritis?
An infectious arthritis caused by bacteria
A chronic autoimmune disease causing synovial inflammation
A degenerative cartilage disorder of the spine
A metabolic condition leading to uric acid crystal deposition
Rheumatoid arthritis is characterized by an autoimmune attack on the synovial lining of joints, leading to chronic inflammation and joint damage. It is not primarily degenerative nor infectious. The hallmark is the immune-mediated synovitis that differentiates RA from osteoarthritis or gout.
Which joints are most commonly affected in rheumatoid arthritis?
Proximal interphalangeal (PIP) and metacarpophalangeal (MCP) joints
Hip and knee joints only
Distal interphalangeal (DIP) joints
Sacroiliac joints
RA typically presents with symmetric involvement of the small joints of the hands, especially the PIP and MCP joints, while often sparing the DIP joints. Larger joints may be involved later, but hand joints are classic early sites. This pattern helps distinguish RA from other arthritides such as osteoarthritis.
Which gender is more frequently affected by rheumatoid arthritis?
Female
Only females
Equal in both sexes
Male
Rheumatoid arthritis occurs more commonly in women than men, with an approximate female-to-male ratio of 3:1. Hormonal and genetic factors are thought to contribute to this disparity. Although men can also develop RA, they do so less frequently.
Morning stiffness in rheumatoid arthritis most often lasts longer than:
15 minutes
5 minutes
30 seconds
60 minutes
Prolonged morning stiffness exceeding 60 minutes is characteristic of inflammatory arthritides like RA, reflecting active synovitis. In contrast, osteoarthritis typically causes stiffness lasting less than 30 minutes. Duration of stiffness is an important clinical clue.
Which autoantibody is most specific for rheumatoid arthritis?
Anti-Smith antibody
Anti-cyclic citrullinated peptide (anti-CCP)
Antinuclear antibody (ANA)
Anti-double-stranded DNA
Anti-CCP antibodies have high specificity (around 95%) for RA and are used clinically to help confirm the diagnosis. They often appear early in the disease course and can predict more severe joint damage. ANA and anti-dsDNA are more associated with lupus.
Which laboratory marker is commonly elevated in active rheumatoid arthritis?
Hemoglobin A1c
Serum creatinine
Erythrocyte sedimentation rate (ESR)
Amylase
ESR is an acute-phase reactant that rises in response to inflammation and is frequently elevated in active RA. C-reactive protein (CRP) is another marker used to assess disease activity. Serum creatinine, HbA1c and amylase are unrelated to inflammatory joint disease.
The pattern of joint involvement in rheumatoid arthritis is typically:
Additive spondyloarthritis
Asymmetric oligoarthritis
Migratory monoarthritis
Symmetric polyarthritis
RA usually presents with symmetric polyarthritis, meaning the same joints on both sides of the body are affected. This symmetric involvement helps distinguish it from other forms such as psoriatic arthritis or gout. Early small joint involvement progressing to larger joints is common.
Which symptom is most characteristic of active rheumatoid arthritis?
Prolonged morning stiffness and joint swelling
Isolated ankle pain only at night
Transient migratory rash
Rapidly resolving back pain
Prolonged morning stiffness lasting more than an hour and persistent joint swelling are hallmarks of active RA. Other symptoms like migratory pain or transient rash are less specific. Recognizing these features aids in early diagnosis and treatment.
What is the significance of anti-CCP antibodies in rheumatoid arthritis?
They are highly specific and predict more aggressive disease
They appear only after 10 years of disease
They indicate viral arthritis rather than RA
They are only elevated in juvenile arthritis
Anti-CCP antibodies are highly specific (around 95%) for RA and can be detected early in the disease course. Their presence is associated with more severe joint damage and can guide treatment decisions. They are not markers of viral or juvenile arthritis.
Which radiographic finding is characteristic of rheumatoid arthritis?
Subchondral sclerosis
Osteophyte formation
Calcium pyrophosphate deposition
Marginal joint erosions and joint space narrowing
RA typically shows marginal erosions and symmetric joint space narrowing due to synovial pannus eroding cartilage and bone. Osteophytes and subchondral sclerosis are features of osteoarthritis, while calcium deposition is seen in pseudogout. Radiographs help differentiate these conditions.
Which extra-articular manifestation is most commonly seen in rheumatoid arthritis?
Malar rash
Calcinosis cutis
Uveitis
Rheumatoid nodules
Rheumatoid nodules are firm subcutaneous lumps often found on pressure points such as the elbows and are the most common extra-articular feature of RA. Uveitis is more common in spondyloarthropathies, while calcinosis and malar rash are associated with dermatomyositis and lupus, respectively.
What is considered first-line disease-modifying therapy for rheumatoid arthritis?
Ibuprofen
Colchicine
Methotrexate
Prednisone
Methotrexate is the anchor DMARD for RA due to its efficacy in reducing disease activity and preventing joint damage. Corticosteroids may be used short-term for flares, and NSAIDs address pain but do not alter disease progression. Colchicine is used for gout, not RA.
Which side effect is most commonly associated with methotrexate in RA patients?
Hepatotoxicity
Renal calculi
Pulmonary fibrosis exclusively
Hyperglycemia
Methotrexate can cause hepatotoxicity, which necessitates regular monitoring of liver function tests. While pulmonary toxicity can occur, it is less common. Renal stones and hyperglycemia are not typical methotrexate side effects.
Which class of biologic agents targets tumor necrosis factor-alpha in RA?
CD20 B-cell depleters
CTLA-4 inhibitors
IL-1 receptor antagonists
TNF inhibitors (e.g., etanercept)
TNF inhibitors such as etanercept, infliximab, and adalimumab specifically block TNF-alpha and are widely used in RA patients who do not respond fully to methotrexate alone. IL-1 blockers, B-cell depleters, and CTLA-4 inhibitors are other biologics with different targets.
Which supplement is routinely given with methotrexate to reduce toxicity?
Calcium
Vitamin D
Vitamin B12
Folic acid
Folic acid supplementation is recommended during methotrexate therapy to reduce side effects such as mucositis and hepatic toxicity. Vitamin B12, D, and calcium are not routinely used to mitigate methotrexate toxicity. This practice improves tolerability and adherence.
What enzyme mediates citrullination of peptides in RA pathogenesis?
Peptidylarginine deiminase (PAD)
Cyclooxygenase (COX)
Tyrosine kinase
Matrix metalloproteinase (MMP)
PAD enzymes convert arginine residues to citrulline, creating neoantigens that drive the autoantibody response in RA. These anti-citrullinated protein antibodies are central to disease pathogenesis. COX and MMPs play roles in inflammation and tissue breakdown, but not citrullination.
Which cytokine is considered a primary driver of inflammation in RA?
Tumor necrosis factor-alpha (TNF-?)
Interleukin-2 (IL-2)
Transforming growth factor-beta (TGF-?)
Interferon-gamma (IFN-?)
TNF-? is a key proinflammatory cytokine in RA, promoting synovial inflammation, pannus formation, and joint destruction. Blocking TNF-? has revolutionized RA treatment. IL-2, IFN-? and TGF-? have roles in immunity but are not primary therapeutic targets in RA.
Patients with rheumatoid arthritis have an increased risk of which comorbidity?
Asthma
Gallstones
Cardiovascular disease
Parkinson's disease
Chronic systemic inflammation in RA accelerates atherosclerosis, leading to higher rates of cardiovascular events. Control of disease activity and traditional risk factor management both reduce this risk. Gallstones, Parkinson's, and asthma are not specifically elevated in RA.
Felty's syndrome in RA is characterized by all EXCEPT:
Elevated rheumatoid factor and rheumatoid nodules
Splenomegaly and neutropenia
Chronic, erosive arthritis
Thrombocytosis
Felty's syndrome is defined by RA, splenomegaly, and neutropenia, often with high rheumatoid factor levels. Thrombocytosis is not a typical feature; patients more commonly have neutropenia. It is associated with severe, erosive joint disease.
Which imaging modality is most sensitive for detecting early synovitis in RA?
Magnetic resonance imaging (MRI)
Conventional X-ray
Bone scintigraphy
Dual-energy CT
MRI is highly sensitive for early joint changes in RA, including synovitis, bone marrow edema, and erosions before they appear on X-ray. Bone scans and CT have roles but are less specific for synovitis. Conventional radiographs detect damage later.
What laboratory monitoring is essential for patients on long-term methotrexate?
Complete blood count and liver function tests
Serum amylase and lipase
Fasting glucose
Thyroid-stimulating hormone
Methotrexate can cause bone marrow suppression and hepatotoxicity, so regular monitoring of CBC and LFTs is mandatory. Pancreatic enzymes, thyroid function and glucose are not directly affected by methotrexate. Close lab surveillance prevents serious adverse events.
Janus kinase (JAK) inhibitors treat RA by:
Inhibiting COX-2 enzyme
Blocking intracellular signaling pathways of multiple cytokines
Neutralizing TNF-alpha in the synovium
Depleting B cells directly
JAK inhibitors such as tofacitinib and baricitinib block the JAK-STAT pathway used by various proinflammatory cytokines in RA. This contrasts with biologics that target single extracellular cytokines like TNF-alpha. They do not act by COX inhibition or direct B-cell depletion.
Sustained remission in RA may allow tapering of DMARDs if the DAS28 score is below:
2.6 for at least 6 months
5.0 for at least 2 years
4.2 for at least 1 month
3.8 for at least 3 months
A DAS28 score below 2.6 sustained for at least six months is considered clinical remission and may justify cautious DMARD tapering. Higher scores indicate low disease activity but not remission. Treatment decisions should always be individualized.
Which HLA allele is most strongly associated with rheumatoid arthritis susceptibility?
HLA-A2
HLA-B27
HLA-DR3
HLA-DRB1*04 (shared epitope)
The HLA-DRB1*04 alleles encode the shared epitope sequence linked to increased RA risk and severity. HLA-B27 is associated with spondyloarthropathies, and other DR and A alleles have weaker or no associations. Genetic predisposition is a key RA factor.
What cellular process leads to pannus formation in rheumatoid arthritis?
Matrix deposition by chondrocytes
Osteoclast apoptosis
Chondrocyte hyperplasia
Synovial fibroblast proliferation with protease-mediated cartilage destruction
Pannus forms from invasive synovial fibroblast-like cells that proliferate and secrete proteases like MMPs, eroding cartilage and bone. This aggressive synovial tissue drives joint destruction in RA. Chondrocytes and osteoclast apoptosis do not create pannus.
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Study Outcomes

  1. Understand RA Symptoms -

    Learn to recognize the hallmark signs of rheumatoid arthritis, including joint pain, swelling, and stiffness. This outcome ensures you can identify early indicators of RA for better self-awareness and prompt care.

  2. Identify Causes and Risk Factors -

    Gain clarity on the genetic, environmental, and lifestyle factors that contribute to RA development. By understanding these triggers, you can better assess personal risk and prevention strategies.

  3. Differentiate RA from Other Joint Conditions -

    Develop the ability to distinguish rheumatoid arthritis from osteoarthritis and other musculoskeletal disorders. This skill promotes accurate conversations with healthcare providers and informed decision-making.

  4. Assess Treatment and Management Options -

    Explore current RA therapies, including medications, physical therapies, and lifestyle modifications. You will learn how different approaches can reduce symptoms and improve joint function.

  5. Evaluate Your RA Knowledge Level -

    Use the quiz results to pinpoint strengths and gaps in your understanding of RA. This reflection helps you focus on areas needing further study or professional guidance.

  6. Apply Insights to Health Conversations -

    Leverage what you've learned to discuss symptoms and treatments confidently with doctors or caregivers. This empowers you to take an active role in your RA care plan.

Cheat Sheet

  1. ACR/EULAR 2010 Classification Criteria -

    The ACR/EULAR 2010 classification criteria for rheumatoid arthritis assigns scores for joint involvement, serology, acute-phase reactants, and symptom duration. A total score of ≥6/10 confirms RA and mastering this scoring system will boost your performance on any rheumatoid arthritis quiz. Familiarity with these criteria is supported by guidelines from the American College of Rheumatology.

  2. Autoimmune Pathophysiology of RA -

    RA is a chronic autoimmune disorder characterized by synovial inflammation and pannus formation driven by Th17 cells releasing IL-17 and TNF-α. The shared epitope on HLA-DRB1 alleles increases susceptibility, a concept detailed in immunology texts at NIH and Mayo Clinic. A handy mnemonic is "SPIKE": Synovial Proliferation Involves Key Enzymes like TNF-alpha.

  3. Classic Clinical Features & Mnemonic -

    Key symptoms include symmetrical polyarthritis in the PIP/MCP joints with prolonged morning stiffness lasting over an hour. The mnemonic "SAD PIP" (Symmetric, Autoimmune, DIP spared, Prolonged morning stiffness) helps you recall the core features when taking an RA quiz. Early recognition of these signs is emphasized in rheumatology reviews at Johns Hopkins.

  4. Laboratory Markers & DAS28 Formula -

    Rheumatoid factor (RF) and anti-cyclic citrullinated peptide (anti-CCP) antibodies are pivotal serologic markers with anti-CCP offering ~95% specificity. ESR and CRP track inflammation levels and are often combined in the DAS28 formula (DAS28 = 0.56√TJC + 0.28√SJC + 0.70 ln(ESR) + 0.014 GH). Mastery of these lab values is frequently tested in "quiz rheumatoid arthritis" challenges.

  5. Treat-to-Target & DMARD Strategy -

    Early, aggressive therapy with disease-modifying antirheumatic drugs (DMARDs) such as methotrexate is the cornerstone of RA management, as outlined by NIH guidelines. The treat-to-target approach aims for remission or low disease activity, often using the mnemonic "MTX before BIO" to remember first-line methotrexate before adding biologics. Understanding this step-up strategy is key to acing your ra quiz.

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