Joint Disorders Flashcards
What is the best way to distinguish joint from soft tissue disorders?
assess active and passive range of motion:
(1) tendon, ligament, bursa, and muscle disorders => affect active ROM
(2) nerve entrapment => active ROM normal/associated with poorly localized pain/burning/parathesia
(3) join disorders => both active and passive ROM limited
What parameters should be assessed in the diagnostic approach to joint pain?
distribution, timing (acute versus chronic), inflammation, extra-articular manifestations
Which joint disorders have a polyarticular (> 4 joints) distribution?
=> rheumatoid arthritis - symmetric, small joints (wrists, hands)
=> lupus - symmetric, small joints
=> viral infections (Hep B and C, EBV, HIV, Parvovirus B19) - symmetric, smaller joints (acute pain - lasts less than 6 weeks)
Which joint disorders have a mono/oligoarticular (1-3 joints) distribution?
=> osteoarthritis - weight bearing joints (hips, knees, lower spine)
=> septic arthritis - monoarticular
=> crystal arthritis (gout [uric acid]/peudo-gout [claclium]) - monoarticular (most common 1st metatarsophalangeal)
=> ankylosing spondylitis - severe back pain in young patients (bamboo appearance of spine)
=> Lyme arthritis
=> psoriatic arthritis
=> arthritis associated with IBD
=> reactive arthritis associated with immune response to bacterial infections (immune/antibody-antigen complexes against bacteria affect joints - it is not the bacteria itself that affects joints)
What distinguishes joint disorders by timing?
(1) monoarticular disorders - osteoarthritis = chronic; gout/septic arthritis = acute; reactive arthritis = subacute
(2) polyarticular - RA and SLE > 6-8 weeks; viral causes <= 6 weeks
What are the characteristics of inflammation in joint disorders?
erythema, warmth, swelling, stiffness (“gelling”) during periods of inactivity (better with exercise, a hot shower, and movement)
What is the best question to ask a patient with arthritis to determine whether condition is caused by inflammation?
how the patient feels first thing in the morning - improvement with activity is indicative of inflammatory arthritis (osteoarthritis is the only arthritic condition that is not inflammatory)
What are the types and characteristics of inflammatory arthritis?
RA, SLE, ankylosing spondylitis, gout, septic => prolonged morning stiffness (> 1 hour), stiffness/pain improves with movement, joint effusion (soft joint swelling/bogginess), redness, warmth, examine joint from sides, ESR/CRP elevated
What are the types and characteristics of non-inflammatory arthritis?
osteoarthritis => no/minimal morning stiffness (< 30 minutes), pain worse with activity, bony crepitus, mild tenderness, hard/bony joint enlargement, NO redness/warmth/effusion, ESR/CRP normal
What are common extra-articular symptoms in joint disorders?
=> SLE - multiple: skin lesions, renal manifestations MUST be present for diagnosis
=> RA - few: skin lesions are unusual and limited to subcutaneous nodules
=> OA - none
=> psoriatic arthritis - skin (plaques) and nails (pitting)
=> HIV/Hepatitis - asymptomatic or multiple systematic symptoms
What is rheumatoid arthritis?
chronic, progressive, autoimmune inflammatory disorder - autoimmune complexes produce cytokines (TNF and interleukins) that recruit more cells to site => leads to proliferation of synovium, erosion of bone, and joint deformities (at advanced stages)
What is the clinical presentation of RA?
symmetric, small joint involvement that spares the distal interphalangeal joints, and lasts >= 6 weeks, morning stiffness (> 1 hour) that improves with activity, joints are swollen/boggy/warm/erythematous, limited active and passive ROM, deformities in advanced disease
What are possible extra-articular manifestations of RA?
very rare: nodules on exterior surfaces, anemia of chronic disease, fatigue, osteoporosis, pleural effusion, pericarditis
=> RA is associated with an increased risk of CV death independent of other risk factors (possibly due to inflammatory response)
How is RA diagnosed?
clinical diagnosis - polyarticular, > 6 weeks duration, not attributable to viral cause or SLE
Which tests support the clinical diagnosis of RA (should never be used as sole criteria for diagnosis)?
=> elevated ESR/CRP
=> + rheumatoid factor (antibodies against one’s own antibodies) - high titers in patients with classic symptoms predicts RA
=> + anti-cyclic citrulinated peptide (peptides are part of normal process of cell death - usually stay within cells but are released from dying cells in RA and produce significant inflammatory response) - indicates both disease presence and severity
=> + abnormalities on x-ray (soft tissue swelling, bone erosions, joint narrowing, small joint effusions, metacarpalphalangeal ulnar deviations, Swan Neck deformities/DIP flexion/PIP hyperextension)
What are the goals of RA treatment?
(1) stop progression of disease (not curable)
2) improve symptoms (minimize pain and improve mobility
Which RA treatments are used to improve symptoms?
NSAIDs +/- steroids:
=> renal disease absolute contraindication for NSAIDs - reduces GFR (give steroids)
=> cannot give steroids long-term (too many side effects)
Which RA treatments are used to slow disease progression (disease modifyng antirheumatic drugs [DMARDs])?
(1) 1st line therapy = methotrexate - dosage is 10X smaller than that given for cancer (does not inhibit DNA synthesis at such small dosage) - contraindicated in pregnancy => need to monitor liver enzymes, CBC, and renal function
(2) TNF inhibitors = adalimubab/Humira and infliximab/Ramicade - more precise mechanism of action (inhibits only one specific protein of inflammation) but much more expensive => must first screen for TB (TNF acts as glue to contain granulomas - giving TNF inhibitors reactivates TB)
