Crystal Arthropathies Flashcards

(44 cards)

1
Q

What is gout?

A
  • common disorder or uric acid metabolism
  • sudden onset of acute flares
  • often in 1st metatarsal pharyngeal joint
  • more common in men as higher uric acid levels
  • peak age is 40-60 for men, 60-80 for women post menopause
  • uric acid levels elevated 20 years before onset
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2
Q

What happens if gout is untreated?

A
  • joint destruction
  • renal damage
  • after first attack there is variable length of time before next attack if untreated
  • second attack longer and more painful
  • time between attacks will get shorter and become more severe = eventually chronic
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3
Q

What is the basic pathophysiology of gout?

A
  • monosodium urate crystals get deposited in small joints
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4
Q

How is it a mostly inert disease?

A
  • urinate crystals in synovial fluid not enough to causy flares
  • crystals normally coated with serum proteins which make them inert (apolipoprotein E/B)
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5
Q

How is it an acute disease?

A
  • when large increase in uric acid

- bone serum proteins don’t have enough time to coat crystals

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6
Q

What happens when there are uncoated crystals present?

A
  • crystals embedded in synovium cause an immune response
  • neutrophils enter joint and phagocytose crystals
  • crystals sharp so neutrophils break
  • release lysosomes, cytokines, IL1 and 8
  • further inflammatory reaction = pain
  • lowering pH by releasing contents so more crystals form
  • repeats cycle
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7
Q

In what joints does it occur more in?

A
  • distal as less blood supply
  • colder and lower pH
  • can often spread to larger joints but rare
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8
Q

What is podagra?

A
  • inflammation of 1st MTP joint
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9
Q

What can it lead to?

A
  • renal damage

- bursitis

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10
Q

What are the features of the joints?

A
  • hot
  • red
  • exquisitely tender
  • pain starts acutely, usually at night
  • initially presents as polyarticular arthritis
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11
Q

What is the significance of intermittent cycles?

A
  • some will have attack again
  • untreated 1st attacks resolve spontaneously in less than 2 weeks
  • lifestyle factor important
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12
Q

What are the features of untreated attacks?

A
  • become polyarticular
  • more proximal and upper extremity joints involved
  • attacks more frequent and last longer
  • chronic polyarticular arthritis almost symmetrical
  • can affect other synovial structures
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13
Q

What are ratphytes?

A

can get erosions outside joint surface (where tendons insert)

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14
Q

What is tophi?

A
  • urate crystals in soft tissues
  • in 50% of untreated gout cases
  • after 10 years develop
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15
Q

What is the histology of gout?

A
  • giant cell reaction to deposited crystals

- tissue macrophage (histocytes) form outer barrier surrounded by lymphocytes

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16
Q

What is uric acid?

A
  • end stage by product of purine metabolism from DNA and RNA from diet
  • mainly in meat, high protein foods = beer/pork/lamb/seafood/beer
  • removed by renal excretion and faeces
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17
Q

What is hyperuricemia?

A
  • when excretion is insufficient to maintain serum urate levels below saturation
  • 6.8ml/dL
  • due to renal insufficiency, dehydration, diuretics
  • rarely related to overproduction of uric acid
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18
Q

What are some risk factors?

A
  • male
  • age
  • obesity
  • ethnicity (pacific islanders)
  • polymorphisms (genetics)
  • kidney disease
19
Q

What causes elevated purine source?

A
  • catabolism of purines
  • tumor lysis syndrome
  • diet
20
Q

What are some hyperuricemia related risks?

A
  • joint inflammation
  • kidney or bladder stones
  • nephropathy
  • CV disease
  • metabolic syndrome
21
Q

What are some causes of decreased renal clearance?

A
  • drugs (aspirin)
  • fructose
  • genetic factors
  • kidney disease
22
Q

What is the gout criteria for diagnosis?

A

11 or more variables:

  • more than 1 attack of acute arthritis
  • max inflammation developed within 1 day
  • monoarthritis attack
  • redness observed over joints
  • first MTP joint painful/swollen
  • tophus
  • hyperuricemia

> or equal to 6/11 = probably gout
4<8 = uncertain, synovial fluid analysis need
<4 = not gout

23
Q

What are the differential diagnoses?

A
  • RA
  • pseudogout
  • septic arthritis
  • reactive arthritis
24
Q

What is the synovial fluid like in gout?

A
  • inflammatory
  • WBC count greater than 2000/ul
  • predominance of polymorphonuclear neutrophils
25
Why is elevated serum uric acid not diagnostic?
- people have it without gout | - only 5-20% of those with gout have it
26
What are the imaging methods?
- x-ray - ultrasound - DEXA
27
What would an x-ray show?
- maintenance of joint space - erosion outside joint capsule - erosion with overhanging edges
28
What would an US show?
- soft tissue swelling | - Doppler = increased blood flow to that joint
29
What would a DEXA show?
- detect uric acid crystal deposits in all late stage gout - detect a lot with early stage too - measure monosodium urate volume and changes following treatment - predict gout flare
30
How would there be joint damage?
- tophaceous deposits= bone erosions - MSU crystals surrounded by granulomatous tissue reaction - produce pro-inflammatory cytokines (IL1,6 TNFa) - stimulate osteoclasts
31
What are the acute treatment methods?
- NSAIDs - colchicine - corticosteroids - IL1 biologicals
32
How should NSAIDs be used?
- start with highest dose for 2-3 days - taper down over 2 weeks - gout symptoms should be absent for 2 days before treatment stopped
33
Why are colchicine second line?
- narrow therapeutic window | - risk of toxicity
34
Who are corticosteroids used for?
- those who cannot use NSAID or colchicine
35
What biologicals should be used?
- riloncept - canakinumab - anakinra - reduce length of attack and reoccurrences - for patients who have severe/frequent flares
36
What are the long term treatment methods?
- allopurinol - probenecid - rasburicase
37
What is allopurinol?
- blocks xanthine oxidase - reduces generation of uric acid - alternative is febuxostat
38
What is probenecid?
- uricosuric - increases uric acid excretion - fewer significant adverse effects
39
What is rasburicase?
- catalyses conversion of acid allantoin
40
What is pseudogout?
- other crystal arthroplasty - calcium pyrophosphate deposition disease (CPDD) - metabolic arthropathy associated with OA - chondrocalcinosis - acute deposition of crystal in and around joints - majority of patients asymptomatic
41
What are the features of pseudogout?
- half of those over 85 have evidence of chondrocalcinosis - pseudo OA with osteophytes and soft tissue calcifications - asymptomatic where only radiographic findings - normally crystals do not interfere with joint - acute = triggered by trauma/reduction of serum calcium = release of calcium in joint, stimulates osteoclasts - knee commonly affected
42
How is pseudogout diagnosed?
- synovial fluid analysis | - US
43
What is synovial fluid like is pseudogout?
- mild to moderate inflammation | - rhomboid shaped weak birefringent crystals
44
What does an US show in pseudogout?
- calcification within soft tissue and articular cartilage - chrondocalcinosis of articular disc/atypical OA of hands - OA in same/neighbouring joints