Crystal arthritis Flashcards

1
Q

the 2 main types of crystal that account for majority of crystal arthritis

A

sodium urate

calcium pyrophosphate

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2
Q

what happens in all crystal arthritis

A

neutrophils ingest the crystals and initiate a pro inflammatory reaction

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3
Q

Gout and hyperuricaemia

A

Gout is an inflammatory arthritis caused by hyperuricaemia and intra-articular sodium urate crystals

Gout is the result of excess uric acid in the body, a condition called hyperuricemia. Uric acid is a substance that normally forms when the body breaks down purines, which are found in human cells and in many foods.

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4
Q

Gout and hyperuricaemia epidemiology

A

common
10x more common in M
FHx of gout

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5
Q

what does hyperuricaemia result from

A

overproduction of uric acid or renal under excretion

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6
Q

where is urate derived from

A

the breakdown of purines (adenine & guanine in DNA and RNA), mainly synthesised by the body

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7
Q

idiopathic gout

A

most common form of gout

most have impaired renal function

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8
Q

In gout, hyperuricaemia and deposition of sodium urate result in 4 clinical syndromes, what are they?

A
  1. acute sodium urate synovitis - acute gout
  2. chronic polyarticular gout
  3. chronic tophaceous gout (A form of chronic gout whereby nodular masses of uric acid crystals (tophi) are deposited in different soft tissue areas of the body)
  4. urate renal stone formation
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9
Q

typical presentation gout

A

middle aged man

sudden severe pain, swelling, redness of metatarsophalangeal joint of the big toe

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10
Q

clinical features gout

A

metatarsophalangeal joint of the big toe
inflam may extend beyond joint giving impression of cellulitis
the urate crystals trigger intracellular inflammation

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11
Q

triggers gout

A

cold, trauma, sepsis, dehydration, dietary (red meat, seafood, fructose intake) or alcoholic excess, starting a diuretic

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12
Q

investigations gout

A
  • joint fluid microscopy: long, needle shaped crystals, negatively birefringent under polarised light
  • serum uric acid raised
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13
Q

immediate management gout

A

first line: NSAIDs eg diclofenac or coxibs
second line: colchicine (narrow therapeutic window & v toxic in OD)
corticosterids, ice, vit C

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14
Q

how further gout attacks prevented?

A

by reducing uric acid levels
obese pts: lose weight
reduce alcohol
thiazides and salicylates should be withdrawn (diuretics)
diet: low calorie and cholesterol, avoid purine rich foods (offal, some fish, spinach)

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15
Q

chronic gout management

A

allopurinol - inhibits xanthine oxidase (enzyme in the purine breakdown pathway) = reduces urate levels rapidly

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16
Q

pseudogout what is it?

A

deposition of calcium pyrophosphate dihydrate in articular cartilage and periarticular tissue

17
Q

radiological appearance pseudogout

A

chondrocalcinosis (linear calcification parallel to the articular surfaces)

18
Q

clinical signs pseudogout

A

shedding of crystals into a joint produces acute synovitis that resembles acute gout
more common in elderly women
effects the knee or wrist

19
Q

pseudogout associated w what other pathologies in young people?

A

haemochromatosis, hyperparathyroidism, Wilson’s disease or alkaptonuria

20
Q

investigations pseudogout

A

joint fluid microscopy - small brick shaped pyrophosphate crystals which are positively birefringent under polarised light (compare with uric acid)
blood count may show raised WCC

21
Q

management

A

joint aspiration
NSAIDs or colchine
injection of local corticosteroids once septic arthritis excluded