common inflammatory arthritis
deposition of monosodium urate crystals
4% over 20 have gout
40% of people with gout have cardiovascular diseae and or diabetes
complex interplay:
genetic
male
maori/polynesian
environmental
stages of gout
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Asymptomatic hyperuricaemia
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biochemical finding
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associated;
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hypertension
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insulin resistance and DM
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kidney disease
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increase cardiovascular risk
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treatmnet not currenlty recommended
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Acute attack
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rapid onset of joint pain
- swelling and eryhtema
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symptoms peak 12-24hrs
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urate levels may be misleadingly normal in 11-49% of people
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Chronic tophaceous gout
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recurrent gout untreated or incompletely managed with urate lowering treatment
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tophi
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more freuqnet anttcks
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increase number of joints involved
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gradual worsening of inlammatory artritis, erosive joint damage and in some cases urate neprhopathy
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communication
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assess patient’s current knowledge
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what have been told about gout
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how noramlly manage acute attack
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build on knowledge
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what gout is
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difference between acute and preventative treatments
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lifestyle aspects
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Check patient has understood
myths
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not all about food
- although etoh(beer), read meat, offal and seafood (shellfish, oily fish), fructose and sucrose sweetned drink
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cann exercise if got gout
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aerobic exerise may temporarily increase urate levels
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but will be beneficial in long term
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cardiovacular risk
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Management
Acute attack
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NSAID
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naproxen 500mg repeated 8-12 hrs then bd on following day tapering dose as attack resolves
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+/- PPI
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Corticosteroids
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prednisone 20-40mg daily gradually reduced over 10-14d
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intra-articular injections if 1-2 joints affected
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colchicine
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(low dose)
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most effective when started early (within 12hrs)
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1mg stat
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0.5mg six hourly
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max 2.5mg/24hrs on first day
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1.5mg on subsequent days
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max 6mg over 4 dyas
- limit prescription to 12 tabs only
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relative CI
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CrCl \<60
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hepatic impairment
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elderly
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weight \<50jg
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Lifestyle
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ideal weight
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2L H2O
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exercise moderatley
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during acute attack;
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rest elevated
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cool
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Include low fat dair, soy, vege sources of protein
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avoid:
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dehydration
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etoh
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foods rich in purines
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soft drinks with fructose or sucrose
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Prophylaxis
achieve urate \<0.36 (lower target 0.3 recommended in some international guidelines)
(in order)
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Allopurinol
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first line
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pharmacology
- block conversion of hypoxanthine and xanthine to urate
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2weeks after acute attack
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concurrent wiht NSAID (250mg bd)
- 3-6 months after achieving serum urate level of ≤ 0.36
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starting dose = 1.5mg per unit of eGFR
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Probenecid
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uricosuric drug
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effective as monotherapy
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start at 250mg bd increase to 500mg bd
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if urate target not achieved
- increase 1g bd
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can combine with allopurinol
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CI in history of kidney stones
- all patients drink 2L /day
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Febuxostat
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80mg od to start - increase to 120mg
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recheck urate 2-4wk after starting
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co-prescribe with lose dose colchicine or low dose NSAID
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monitor LFT - initiiation then 1-3 mo after starting
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mechanism/pharmacology
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potent
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non purine
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selective inhibitor of xanthine oxidase
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inhibits production of uric acid
- prevents normal oxidation of purines to uric acid
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similar mechanism to allopurinol but more potent
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half life = 5-8hrs therefore suitable for once daily dosing with or without food
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Special authority
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patient >0.36 urate despite allopurinol 600mg/day and probenecid
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or intolerable side effects
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or both:
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renal impairment and urate >0.36 despite optiaml therapy and
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CrCl ≤ 30ml/min
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adverse reactions:
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naeusa
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diarhroea
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headache
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rahs
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gout flares
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LFT abnormalities
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ALT 3x ULN
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?lcincal signifiance
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request LFT prior to starting
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use with caution
- cardiovascualr disease
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prophylaxis essential during treatment initiation
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ddoesn’t need dose adjustment mild - mod renal impairment
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> 30mL/min
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eliminated both liver and renal
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Benzbromarone
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uricosuric agent
- increase urate excretion by kidney
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100-200mg more effective than 1g probenecid daily
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similar to 300-600mg daily allopurinol
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mesaure LFTs frequently
- montly first 6mo at least
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more effective ?in polynesion
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special aurthority
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section 29 - need patient consent
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