Week 2 Crystal induced arthopathies Flashcards

1
Q

List the crystal species and their associated arthritic disorders.

A
  1. Monosodium urate- Gout
  2. Calcium pyrophosphate - Pseudogout
  3. Hydroxy apatite - Calcific periarthritis
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2
Q

Describe the inflammation response to crystals.

A
  • stimulate release of inflammatory mediators: arachidonic acid, Il-1,6,8, TNF
  • granulocyte influx promoted
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3
Q

What are the clinical features of gout?

A

-arthritis
-tophi
-kidney stones
-nephropathy
Presentation
-intermittent attacks, initial symptoms peak at 12 hours, first MTP (big toe) joint affect frequently initially. Inflammation and marked pain.
-sodium urate crystals initiate the acute attack, need shaped and show negative birefringence
-attack will last a few days or weeks and subside
-systemic symptoms, fever and chills
-recurrent attacks
-tophaceous deposits over time

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4
Q

Who does gout affect?

A
  • 8.4/1000 ppl
  • those with renal impairment
  • lipoprotein abnormalities
  • increasing body mass
  • excessive alcohol consumption
  • familial gout 20%
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5
Q

Describe tophaceous gout (chronic gout).

A
  • generally 10 years+ of gout
  • no longer pain free between attacks
  • subQ deposits of urate accumulate, without treatment 50% will develop tophi
  • may occur in abnormal places: spine and CNS
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6
Q

What are radiographic features of gout?

A
  • x rays generally normal early on
  • soft tissue swelling during acute attacks
  • gouty destruction of bone characteristics: erosions slightly removed from joint surface, atrophic and hypertrophic features result in overhanging edge appearance
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7
Q

How is acute gout treated? How is hyperuricemia treated?

A
  1. Colchicine-effect in early attacks and to prevent attacks during asymptomatic intervals
  2. NSAIDS
    Hyperuricemia
  3. Uricosuric drugs: contraindicated in patients with over excretion of uric acid
  4. Allopurinol-inhibits xanthine oxidase
  5. diet
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8
Q

What is calcium pyrophosphate dehydrate crystal deposition disease (CPPD)?

A
  • pseudogout
  • gout like attacks
  • may mimic other conditions such as RA and septic arthritis
  • crystal accumulate in cartilage
  • chondrocalcinosis on x ray
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9
Q

Describe the clinical features of pseudo gout.

A
  • acute attacks 3-14 days
  • self limited but respond to treatment
  • predilection for larger joint involvement compared to real gout
  • first attack knee joint 50%
  • nearly all joints can be affected
  • asymptomatic between attacks
  • low grade fever common with acute attacks
  • chronic symptoms in some patients: OA of knees, pseudo rheumatoid polyarthritis
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10
Q

What are CPPD disease associations (associations with chondrocalcinosis)?

A
  1. Hyperparathyroidism ! most notable
  2. hemochromatosis
  3. hypothyroidism
  4. hypomagnesemia
  5. hypophosphatasic
  6. amyloidosis
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11
Q

What are radiographic features of CPPD?

A
  1. calcifications visible on plain films
  2. generally linear calcific densities in cartilage
  3. may occur in joint capsule, ligaments, tendons, isolated patellofemoral arthritis, or wrist degeneration
    - If see medial or lateral meniscus deposition of calcification if patellafemoral
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12
Q

How is CPPD treated?

A
  • No practical way to remove CPPD crystals from cartilage
  • Treatment of associated conditions does not remove crystals
  • Local treatment of acute affected joints with aspiration and steroid injection helpful
  • oral ant inflammatory medications and/or colchicine generally effective
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13
Q

Describe basic calcium phosphate crystal deposition disease.

A

-acute and chronic calcific periarthritis
-large joint destruction arthritis
-calcinosis cutis
-may cause local inflammation
-generally more periarticular symptoms
-crystals: apatites, tricalcium phosphate, octacalcium phosphate
Diagnosis:
-tendonitis
-softe tissue calcifications on x ray
-crystals can’t be confirmed with polarizing microscope
-coin like clumps may be seen with light microscope
Treatment
-NSAIDs, local injection with corticosteroid, physical therapy

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14
Q

What conditions are associated with urate overproduction?

A
  • HGRFT deficiency: in the purine salvage pathway
  • PRPP synthetase superactivity: in the de novo purine synthesis
  • myeloproliferative disease
  • hemolysis
  • psoriasis
  • glycogen storage disease
  • ethanol
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