Rheumatic Diseases Quiz

Rheumatic Diseases and Their Characteristics

• Rheumatoid factor autoantibodies do not indicate infection, infective process, or enzymatic defect.
• Rheumatoid arthritis is associated with systemic aching in the musculoskeletal system, debilitating joint pain and stiffness, and changes in daily activities.
• Systemic lupus erythematosus (SLE) is attributed to autoimmune mechanisms, not wear and tear on weight-bearing joints or septic joint inflammation.
• SLE leads to numerous complications due to immune injury to basement membranes.
• A positive antinuclear antibody test helps confirm the diagnosis of SLE.
• Patients with SLE should avoid sun exposure to prevent the progression of cutaneous lesions.
• The classic presentation of SLE includes a butterfly pattern rash on the face, not lesions on the palms and soles, dry scaly patches, or cracked scaly areas.
• Ankylosing spondylitis is characterized by inflammation, stiffness, and fusion of spinal joints.
• Prosthetic joint infection is often due to bacterial spread to the joint via the bloodstream, not defective replacement material, joint injury, or arthritis.
• Scleroderma involves fibrosis of connective tissue, not autoantibodies against acetylcholine receptors, infection by beta-hemolytic streptococcus, or inflammation caused by antigens.
• The earliest manifestation of scleroderma is Raynaud phenomenon with blanching of the digits in response to cold.
• The most common presenting sign/symptom with rheumatic fever is polyarthritis, not cardiac murmur or rash.

Pathophysiology of Gout, Rheumatoid Arthritis, Ankylosing Spondylitis, and Osteoarthritis

• The final chronic stage of gout is called tophaceous gout characterized by crystalline deposits in cartilage, synovial membranes, and soft tissue.
• In rheumatoid arthritis, immune cells accumulate in pannus and destroy articular cartilage.
• Gout occurs when uric acid crystals form in joints; calcium phosphate and beta-hydroxybutyric acid do not lead to crystal formation in gout.
• Ankylosing spondylitis causes joint fibrosis, ossification, and fusion, most commonly of the intervertebral and sacroiliac joints.
• The chief pathologic features of osteoarthritis are degeneration of articular cartilage, destruction of the bone under the cartilage, and thickening of the synovium.
• Osteoarthritis involves a complex interaction between osteoclasts, osteoblasts, chondrocytes, and synoviocytes that eventually destroy cartilage and damage subchondral bone.
• Characteristics of gout include disturbed uric acid metabolism, crystalline deposits in bony and connective tissue, and cardiac and renal involvement.
• Manifestations of osteoarthritis include nodules on joints of the hands, crepitus with joint movement, and narrowing of joint spaces.
• Signs/symptoms of Lyme disease include fever and chills, arthritic pain, headache, and myalgia, but not migratory rash.
• Gouty arthritis and complicated gout are not the final stages of gout; asymptomatic hyperuricemia is the first stage of gout.
• In ankylosing spondylitis, there is no costal cartilage degeneration, instability of synovial joints, or temporomandibular joint degeneration.
• The pain in osteoarthritis is worse with activity and is relieved with rest; stiffness is relieved with joint use.