Gout

Question 1

Pathogenesis

Answer 1

deposition of urate crystals within a joint
usually a result of hyperuricaemia = high serum uric acid
uric acid is the final compound in the breakdown of purines in DNA metabolism (A&G)
uric acid crystals precipitate in joints - triggered by dehydration, trauma, surgery

Question 2

what causes hyperuricaemia?

Answer 2

(high serum uric acid = hyperuricaemia)
renal excretion (can be exacerbated by diuretics/renal failure)
excessive alcohol intake 
excessive red meat 
excessive seafood

Question 3

who gets it?

Answer 3

there is some evidence of predisposition for gout

Question 4

how does it present?

Answer 4

1st MTP joint is classic site - Podagra
ankle and knee also common
intensely painful, red, hot swollen joint - mimic septic arthritis
7-10 days if untreated to resolve
gouty tophi
chronic gout - destructive erosive arthritis

Question 5

what are gouty tophi?

Answer 5

painless white accumulations of uric acid in soft tissues

occasionally erupt through the skin

Question 6

how is it investigated?

Answer 6

sample of synovial fluid
analysed with gram stain and culture to exclude infection
polarised microscopy
- needle shaped uric acid crystals
- -ve birefringence (change from yellow to blue when lined across the direction of polarization)

Question 7

how is it managed?

Answer 7

acute attacks
- NSAIDs (colchaine for patients who can’t tolerate NSAIDs)
- corticosteroids
- opioid analgesics
recurrent attacks/ joint destruction/ tophi
- allopurinol or other urate lowering therapies once the acute attack has settled (they can potentiate a further flare)