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)
What is systemic lupus erythematous (SLE)?
autoimmune disease against one’s own DNA with multiple organ involvement (complexes deposit in multiple organs) - follows a relapsing and remitting course (unpredictable flares) => non-erosive arthritis
What is the progression in SLE?
genetic and environmental triggers cause an abnormal immune response that result in the formation of auto-antibody immune complexes => inflammation and organ damage (renal failure, pulmonary fibrosis, and stroke)
What is the clinical presentation of SLE?
=> skin manifestations (70%):
- acute malar (butterfly) rash, alopecia, painless oral ulcers
- chronic discoid rash (raised edges/leaves scars)
- subacute photosensitivity rash (sun exposed areas/”sunburn” that lasts months)
=> lupus nephritis (70%)
=> less common: arthritis, cardiac and pulmonary manifestations, CNS abnormalities (headaches, cognitive/behavioral dysfunction, depression, seizures), hematologic manifestations (anemia, thrombocytopenia, leukopenia), constitutional (fatigue, weight loss, fever, myalgia)
How is SLE diagnosed?
clinical diagnosis
Which tests support the diagnosis of SLE?
=> + anti-nuclear antibody (antibody against one’s own DNA) - hallmark of SLE (should be initial test)
=> + anti-dsDNA (antibodies against double stranded DNA) - used to confirm the diagnosis if ANA is + (most specific diagnostic test)
=> decreased complement level in SLE flare
=> x-ray negative (non-erosive arthritis)
What is lupus nephritis?
deposition of immune complexes/proteins in glomerular capillary membrane - need to test for proteins in urine (cannot use urine dip since dip only detects microalbuminuria)
How is lupus nephritis diagnosed?
initial tests and monitoring:
=> serum for creatinine/GFR
=> urinalysis for protein and RBCs (dysmorphic - change in shape of RBCs)
=> 24 hour urine collection for urine protein (perform if protein or RBCs detected)
definitive diagnosis:
=> renal biopsy - used to determine approach to therapy
What is the treatment for SLE?
acute exacerbations - corticosteroids
maintenance/prevention:
=> sun screen
=> hydoxycholoroquine (Plaquenil) for skin rashes, arthritis, and prevent flares
=> cytotoxic drugs (cyclophosphamide IV) for severe lupus nephritis
What are the side effects of methotrexate?
GI upset, liver toxicity, marrow suppression
=> monitor CBC, liver function, renal function
=> screen for viral hepatitis prior
=> contraindicated in pregnancy (folate antagonist)
What are the side effects of TNF inhibitors?
reactivation of latent TB, fungal and bacterial infections
=> screen for TB, HIV, viral hepatitis prior - repeat TB screening annually
=> low risk in pregnancy - should be continued
What are the side effect of hydroxycholoroquine?
retinal damage - rare but irreversible => requires fundoscopic exam by specialist prior and annually
What is osteoarthritis?
degenerative/non-inflammatory disorder affecting cartilage (wear and tear), progressive (increases with age), affects weight bearing joint (knees, hips, lumbar spine), can affect distal interphalangeal joints
What are the clinical manifestations of OA?
monoarticular/oligoarticular joint involvement, pain relieved by rest/worse with activity, morning joint stiffness < 30 minutes, hard/bony enlargement, crepitus, limited ROM (active and passive), no systemic symptoms
How is OA diagnosed?
clinical diagnosis
Which tests support a diagnosis of OA?
normal ESR/CRP, abnormalities on x-ray (joint space narrowing, osteophytes/bone overgrowth, subchondral bone damage/sclerosis, NO bone erosions)
What are the common joint abnormalities in OA?
Bouchards nodes (proximal joints) and Heberden’s nodes (distal joints) = B before H (Bouchards nodes are proximal)
What is the treatment for OA?
=> weight loss
=> regular exercise to improve joint ROM and muscle strength
=> start with acetaminophen - NSAIDs (topical or oral)
=> intra-articular injection (no more than 3-4 per year)
=> surgery only for serious disability
=> nutritional products (OTC glucosamine and chondtrotin sulfate) show NO good evidence of benefit
What is gout?
NOT a joint disorder - metabolic disorder
=> manifestation of hyperuricemia (increased production or decreased excretion)
=> deposition of monosodium urate crystals in lower joints because needs lower temperature
=> more prominent in patients with chronic renal disease (uric acid cannot be excreted by kidneys)
=> most commonly 1st metatarsophalangeal joint (base of the great toe/podagra)
Which substances can precipitate a gout attack?
=> beer, red meat, seafood
=> medications - niacin, thiazides, ASA
What is the mechanism of formation of uric acid?
byproduct of purines (nucleic acids) - any release of DNA causes increase in purines => foods with a lot of cells and cells with high turnover rates (cancer) produce more purines
What are the manifestations of gouty arthritis?
sudden onset of exquisite joint pain (often wakes from sleep), inflammation (redness, warmth, swelling, tenderness), tophi (aggregation of urate crystals under the skin - occur in recurrent and poorly controlled gout)
How is gout diagnosed?
=> elevated serum uric acid (can be normal in 25% of patients)
=> x-ray normal during early stages (bone erosions in chronic/recurrent gout)
=> elevated ESR/CRP - non-specific
=> diagnostic = aspiration of synovial fluids (WBCs 5,000-50,000 cells with neutrophils < 75% and needle-shaped crystals on microscopic exam)
What are the results of synovial fluid analysis in OA, gout, and septic arthritis?
(1) OA: WBCs < 5,000; PMN < 25%, negative for crystals
(2) gout/pseudo-gout: WBCs 5,000-50,000, PMN > 50%, needle-shaped crystals (gout) or rhomboid crystals (pseudo-gout)
(3) septic arthritis: WBCs > 50,000, PMN > 75%, negative for crystals
How is the clinical diagnosis of gout made?
the presence of more risk factors increases the confidence in the diagnosis (joint aspiration only if needed - requires vigilant follow-up due to possibility of joint erosion):
- acute onset (maximal symptoms within one day)
- joint erythema
- Hx of chronic kidney disease
- male patient
- previous attack of arthritis/joint pain
- 1st metatarsophalangeal joint involved
- serum uric acid > 6 mg/dl
What is the treatment for an acute attack of gout?
=> NSAIDs +/- Colchicine (anti-inflammatory - used for acute flares) - reduce doses or avoid in patients with renal disease
=> steroids - if poor response to initial therapy or for patients with renal insufficiency
What is preventive therapy for gout attacks?
=> reduce intake of alcohol (especially beer) and high purine foods (red meat, organ meat, seafood)
=> urate lowering medications if > 2 attacks per year
What are the urate lowering medications used in the treatment of gout?
drugs that decrease production of uric acid to prevent flares:
=> allopurinol (1st line) - prevents conversion of purine to uric acid (reduces the amount of uric acid in the blood - purines remain in the blood but are used for DNA synthesis)
=> febuxostat (Uloric) - used in patients who cannot tolerate allopurinol
drugs that increase excretion of uric acid from the kidney:
=> probenecid - less effective and contraindicated in renal insufficiency
How is urate lowering therapy implemented?
initiated between flares (use during an attack can incrase uric acid levels and worsen attack) - start low and titrate to uric acid level < 6 mg/dl (crystals form at uric acid levels higher than 6 mg/dl)
