gout Flashcards
what is gout caused by
imbalances in purine metabolism and deposition of monosodium urate crystals in articular and periarticular tissues
what are the types of gout
acute
- recurrent acute gouty arthritis
chronic
- tophi (depositions of MSU crystals in tissue and surrounding joints)
- interstitial renal disease (gouty nephropathy)
- uric acid nephrolithiasis (uric acid kidney stones)
what are the risk factors of gout
dietary and lifestyle factors
- alcohol consumption
- sugary beverages
- red meat
- sedentary lifestyle
- obesity
gender (M>F)
what is the pathophysiology of gout
purine is metabolised into waste products like guanine and adenosine which would be converted into hypoxanthine, converted into xanthine by xanthine oxidase and eventually into uric acid by xanthine oxidase and excreted
factors resulting in over-production of uric acid
- excessive alcohol consumption
- excessive purine consumption
- excessive fructose
- cytotoxic drug
factors resulting in under-excretion of uric acid
- diuretics
- levodopa
- low dose aspirin
- cyclosporin/ tacrolimus
- ethambutol
- ethanol
- pyrazinamide
- laxative abuse
- nicotinic acid
- salt restriction
what is the presentation of gout and of a gout attack
gout
- monoarticular
- asymmetrical
- pain (excruciating, rapid onset)
- assoc sx (swelling +++, tenderness +++, erythema +++)
- deformities (tophi)
- diagnostics (increased serum uric acid, joint aspirate shows urate crystals and increased WBC)
gout attack
- monoarticular
- asymmetrical
- wakes up from sleep due to pain
- severe excruciating pain for several hours
- rapid onset (usually overnight)
- swelling and discomfort continues days to weeks after
- joint is red, hot, swollen and presence of tophi
what are the goals of therapy of gout
- provide rapid, safe and effective pain relief
- prevent future attacks by reducing SU conc
- address associated comorbidities
- prevent joint destruction and tophi formation
- increase QoL
what is considered hyperuricemia
uric acid >6mg/dL for female and >7mg/dL for male
what is the management strategy for acute gout flare
- to treat asap, within 24hr
- first line is colchicine 1mg LD f/b 0.5mg 1hr later
- alternatively is PO celecoxib 400mg LD f/b 200mg 12hr later f/b 200mg BD x5-7d
- or alternatively is PO prednisolone 30-40mg OD x2-5d f/b taper by halving dose x7d f/b discontinue
- monitor by measuring serum SU conc, assess lifestyle and comorbs, medication review and consider ULT
when should ULT be initiated
- freq acute gout flares (2 or more a year)
- presence of tophi
- clinical or imaging findings of gouty arthropathy
- hx of urolithiasis
how to initiate ULT after an acute gout flare
- 2-4w after gout flare has settled
- anti-inflamm prophylaxis 3-6m w colchicine 0.5mg OD or low dose PO celecoxib 200mg OD or low dose PO prednisolone 5-7.5mg OD
what is the treatment target for ULT
- <6mg/dL for non-tophaceous
- <5mg/dL for tophaceous
what are the agents used for ULT and how do they work
- allopurinol (xanthine oxidase inhibitor to decrease uric acid synthesis)
- febuxostat (xanthine oxidase inhibitor to decrease uric acid synthesis)
- probenecid (URAT1 and GLUT9 inhibitor to increase uric acid excretion)
what are the concerns with each of the ULT agents
allopurinol and febuxostat risk of SCAR (F < A)
probenecid should be avoided in CrCl <50 and ensure adequate hydration
what is the dosing regiment like to initiate ULT
allopurinol
- initiate 100mg/d or lesser f/b titrate up 50-100mg q2-8w to MD of 300mg/d or less (max 800mg/d for normal renal function)
febuxostat
- initiate 40mg/d or lesser f/b titrate up to 80mg/d in 2-4w if not yet at target
probenecid
- initiate at 250mg BD x1w f/b 500mg BD f/b titrate up 500mg q4w to 2g/d or less
what is the acronym that indicates higher risk of SCAR associated with allopurinol
R enal impairment
A gent (concom use of diuretics)
S tarting dose high
H LAB*5801
E scalation of dose
S eniority
