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Gout
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<<forEachTiddler where 'tiddler.tags.contains(context.inTiddler.title)' sortBy tiddler.title ascending write '"*[["+tiddler.title+"]]\n"'>> <<tiddler AutoRefresh with: force>> Microcrystal synovitis - Monosodium urate crystal deposition esp in joints, kidneys and other soft tissue caused by chronic hyperuricaemia (urate >450) typically mono-arthritis (esp 1st MTP in foot) M=F post 60yrs, pre-men F less esp african inc with age dietary component Uric acid crystal depostis are tophi which grow and cause bone erosion and painful damage Uric acid is end product of purine metabolism, produced by liver and excreted by kidney 90% gout - due to difficulty excreting urate, 10% due to overproduction may have hyperuricaemia for 20 yrs before Sx start aSx - urate usually coated with apolipoprotein so don't bind to cell surface, in gout this gets dissolved off and an immune response follows - so Rx recoats the urate and Sx resolve ''risk factors'' envt, diet, genetics obesity and insulin resistance may contribute drugs - aspirin, diuretic ''Clinical criteria'' 1st MTP involved severe joint pain develops over 6-12 hrs swelling, tender, erythema self limiting - resolves completely tophus ''Ix'' serum urate not in acute phase (Sx due to acute change in urate level - so dec impt as well), WCC and CRP may be useful acutely TG LDL - associated with gout fasting glc baseline U/E 24 hr urine for urate (over excretors of urate won't respond to uricosuric therapy, most pts with high serum levels are unable to excrete) ?MC&S of joint fluid if thinking sepsis ''2ndary gout'' underexcretion - hypothyroid, hyperparathyroid, nephropathy, dehydration, chronic alcohol, drugs (thiazides) overproduction - diet, obese, high cell turnover, myeloproliferation, psoriasis, chemo, anaemia (haemolytic and pernicious), xs exercize ''Treatment'' - do NOT treat aSx hyperuricaemia ''Acute'' therapy - NSAID, Intra-articular steroids, Colchicine, prednisolone (all 2/52 and taper) ''Prophyllaxis'' - if >2 attacks per year (high urate), start >2/52 after acute phase, uricosuric (Probenecid, amlodipine, atorvastatin, Losartin), Xanthine oxidase inhibitors (Allopurinol) aim - minimise morbidity and decrease disabling end organ damage - use with thought of SE with age reduce urate load (avoid liver, kidney, seafood, oily fish, yeast) lifestyle - reduce alcohol and weight ''Colchicine'' slow onset action 80% GI SE (usually diarrhoea) avoid if eGFR <60 (or half dose) ''Allopurinol'' can precipitate attack if start early (<2/52 after acute) Initial 100mg od and inc till urate <300 cover start with NSAID or colchicine use if >2 attacks in year, tophi, renal disease, urate stones, on cytotoxics or diuretics Allopurinol use if tophi, Xray changes, 2+ attacks /yr, uric acid nephropathy or stones cover start with NSAID for 1-3/12 - until hyperuricaemia is corrected (to avoid ppt an attack) if attack on allopurinol keep dose same until resolved and then titrate up SE - rash diarrhoea nausea also .... lots ! alternative - Febuxostat (beware liver disease and CCF) Probenecid - fewer SE, less effective, avoid if renal stones / impaired, on aspirin and with CCF as need to drink lots Other drugs (above) are all mildly uricosuric Diet liver, kidney, red meat, herring, sardines, salmon tomatoes, celery, new potatoes, spinach, strawberries Caviar, Beer, 10% initial presentation is polyarticular (esp elderly women with renal impariment) In time attacks are generally less severe but more frequent and prolonged more proximal and polyarticular Renal stones more common in gout esp pure uric acid stones leads to renal impairment Tophi acute gout linked to mental health issues - renal failure and arthritis documented in all tissues except brain
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