Gout Flashcards
presentation
acute monoarthropathy with severe joint inflammation
>50% at MTP of the big toe
pathophysiology
deposition of monosodium urate crystals in and near the joints
can be precipitated by trauma, surgery, starvation, infection or diuretics
ass. w/ raised plasma urate
in the long term, urate deposits (= tophi, eg in pinna, joints, tendons) and renal disease (stones, interstitial nephritis) may occur
DDx
exclude septic arthritis
haemarthrosis
pseudogout (calcium pyrophosphate deposition)
RA
causes
hereditary increased dietary purines alcohol excess diuretics leukaemia cytotoxics (tumour lysis)
associations
CVD
HTN
DM
chronic renal failure
gout is a marker for these, so seek and out treat if needed
investigations
polarized light microscopy of synovial fluid shows NEGATIVELY BIREFRINGENT urate crystals
serum urate is usually raised but may be normal
radiographs show only tissue swelling in the early stages
later, well defined, punched out erosions seen in juxta-articular bone
no sclerotic reaction
joint spaces preserved until late
Tx
high dose NSAIDs or coxib (eg etoricoxib)
Sx should subside in 3-5d
rest and elevation
prevention
lose weight
avoid prolonged fasts, purine rich meats and low dose aspirin, which raise serum urate
aim to reduce joint damage and reduce number of attacks
use allopurinol
calcium pyrophosphate deposition (CPPD)
umbrella term for the following:
acute CPP crystal arthritis (pseudogout) - like gout
chronic CPPD - inflammatory RA-like polyarthritis and synovitis
osteoarthritis with CPPD - OA with superimposed CPPD attacks
risk factors:
old age, hyperaldosteronism, haemochromatosis, hypophosphataemia
tests:
POSITIVELY BIREFRINGENT crystals
management CPPD
acute:
ice packs, rest, aspiration, intra-articular steroids
NSAIDs +/- colchicine
methotrexate and hydroxychloroquine also have a role in chronic CPPD
