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32 Cards in this Set
- Front
- Back
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crystal arthritis
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-Crystalline arthritis can be acute or chronic and involve multiple joints
-Inflammation is due to the interaction between phagocytes and crystals |
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crystal
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1. monosodium - gout
2. Ca pyrophosphate - pseudogout 3. basic Ca phosphate - Calcific periarthritis Sub acute arthritis "Milwaukee shoulder" |
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gout
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-inflamm process in joints or periarticular tissue
-results from tissue deposition of monosodium urate crystals -predominantly a dz of adult men (after menopause in W incidence is equal) -rare in pre-menopausal women |
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purines
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-bases derived from dietary + endogenous sources
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uric acid
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-- the natural end product of purine metabolism.
-stays soluble in plasma up to 6.7mg/dL. -largely excreted by the kidneys. |
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hyperuricemia
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-best defined as a serum uric acid level ≥6.8mg/dL
-Humans lack uricase which oxidizes insoluble uric acid to the much more soluble allantoin. -Yet not all hyperuricemic subjects develop gout. |
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causes of hyperuricemia
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-overproduction: <10% of hyperuicemia and is caused by:
1. inherited disorders of purine nucleotide biosynthesis 2. rapid cell turnover 3. excessive dietary purine intake -underexcretion- most common cause -mixed- beer! |
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underexcretion seen in
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-renal insufficiency from diabetes, hypertension.
- lactic acidosis, ketoacidosis. - diuretic use - dehydration -cyclosporine -lead poisoning |
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acute gout clinical pres
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- Acute attack of intense pain – usually in lower extremity joints – following trauma, dietary indiscretion, dehydration or acidosis
- Twinges of discomfort progress to severe pain over 8-10 hours with clinical evidence of synovitis -Commonly affects the great toe (podagra), knee, mid-foot, wrist, and elbow. -Rare reports in the spine. |
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other features of acute gout
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-fevers, chills
-Serum urate levels fall during acute gout often resulting temporarily in a “falsely normal” value.1 -Weight bearing is often impossible with the acutely inflamed joint. -Attacks last for 4 to 8 days in the early phases and up to 2 weeks as time passes. |
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advanced gout
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-With time and sustained hyperuricemia, gout can become polyarticular.
-Renal stones occur in 25% of gouty subjects -Subcutaneous tophi can develop over extensor surfaces. These are firm nodules of urate crystals surrounded by a foreign body granuloma. -Chronic tophaceous gout can cause erosions and deformity. -tophi, chronic pain and deformities cardinal features |
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presumed gout
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- a “soft” diagnosis based on a history of acute, intermittent, monoarthritis in the setting of hyperuricemia with or without a clinical response to colchicine.
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definitive gout
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-microscopically proven MSU crystals in synovial fluid or tophi
-In the acute attack, these are intracellular, needle shaped crystals with strong negative birefringence -Small, “chewed up” extracelluar crystal fragments are seen late in attacks or between attacks |
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lab findings
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-Elevated synovial fluid WBC is noted in most infectious and crystal induced arthritis.
-Crystals observed in synovial fluid do not rule out infection. -Fluid culture and examination under a polarized light microscope is essential to confirm diagnosis. -Elevated sedimentation rate (often impressive) is seen in acute gout but has no specificity |
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serum urate...
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-might be low during a flare. Recommend performing after the flare has subsided. 2-3 weeks.
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radiographic findings
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-plain xrays
-Early in disease process Soft tissue swelling, no erosions - Classic mid to late stage findings: “overhanging edges” and asymmetric erosions. |
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tx of acute attack
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-NSAIDs
-Colchicine -steroids |
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Indications for Treatment of Hyperuricemia
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-recurrent attacks of gout = >2/yr
-xray evidence of erosive dz -presence of tophi |
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chronic therapy
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-Maintaining patient in a symptom-free state while reducing serum urate to less than 6.0 mg/dl
-low dose daily NSAID or colchicine 0.6 mg QD-BID until the goal is met for several months. |
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urate lowering drugs
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-allopurinol
-febuxstat -probenecid |
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best urate lowering strategy
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Begin with allopurinol at 100mgs a day or febuxostat at 40mgs a day
Hold the dose there for a month Repeat a serum urate level and titrate dose up by 50-100 mg in the use of allopurinol or 80mgs in the use of febuxostat. Repeat this step until treatment goal is achieved. Goal is a serum uric acid of <6.0mgs/dL |
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Non-pharmacologic approaches to urate lowering
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-Lifestyle modification such as weight loss, low-purine diets, abstinence from alcohol, management of co-morbidities are essential.
-to reduce dietary purine burden avoid foods like: shellfish, small fish, organ meats, beer |
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Calcium Pyrophosphate Dihydrate (CPPD) Deposition Disease
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-form of crystalline arthropathy is manifested by CPPD deposition in cartilage and synovial tissues and marked heterogeneity of clinical presentations.
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Clinical Presentation of CPPD Deposition
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Acute mono-arthritis (pseudogout)
Polyarticular noninflammatory arthritis (pseudoOA) Polyarticular inflammatory arthritis (pseudoRA) Neuropathic-like joint destruction (pseudo-Charcot) Asymptomatic |
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CPPD dx
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1. synovial fluid analysis:
-Rhomboid or rectangular shaped crystals with weak positive birefringence -Dominant cell type - neutrophils 2. Xray findings: -Punctate linear deposits of CPPD --crystals in the menisci and cartilage -called chondrocalcinosis |
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CPPD tx
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-No therapy is available to deplete the crystal burden. Non steroidal anti-inflammatory agents moderate symptoms.
-Oral colchicine -Intra-articular corticosteroids often help in acute setting. |
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Basic Calcium Phosphate (BCP)
Hydroxyapatite Deposition Disease |
-Caused by deposition of calcium phosphate crystals (hydroxyapatite) in cartilage and peri-articular structures such as tendons.
-older women |
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Clinical Manifestations of BCP Disease
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Non-inflammatory destructive arthropathy -
“Milwaukee“ shoulder Acute inflammatory arthritis - like gout or pseudogout Acute calcific periarthritis - hips and shoulders in middle-aged and older women Osteoarthritis with BCP crystals – accelerated joint destruction in OA Diffuse Idiopathic Skeletal Hyperostosis (DISH) – elderly or middle-age men. May be asymptomatic |
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“Milwaukee” Shoulder
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-Large non-inflammatory effusion with gleno-humeral instability. Usually in elderly women.
-High-riding humeral head with remodeling of the acromion, clavicle and superior humerus |
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BCP labs
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-Synovial fluid is generally non-inflammatory
-No helpful serum biomarkers -BCP crystals are not birefringent and can not be seen by regular microscopy unless in clumps (“shiny coins”). These clumps will stain with alizarin red S stain (next slide). -Can co-exist with CPPD crystal disease |
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treatment
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-treatment is generally unsatisfactory because of the degree of destruction at diagnosis. NSAIDs and intra-articular steroids may be helpful. Repeat aspiration and physical therapy are often necessary.
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Cholesterol Crystals
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- not phagocytized nor associated with inflammation
- found in chronic effusions, esp. bursal |
