Gout Flashcards
what is gout?
purine metabolism disorder
crystal arthropathy from excess levels of uric acid leading to precipitation in joints and other tissue
epidemiology of gout
most common inflammatory arthritis across the world
prevalence is increasing
more common in elderly
males more at risk
what are the risk factors?
high uric acid levels/ hyperuricaemia alcohol obesity male age renal disease dyslipidaemia chemotherapy diabetes mellitus
what is uric acid?
breakdown product of purines
excretion of uric acid
predominantly renally excreted and the rest excreted via GI tract
imbalance between production and excretion of uric acid it may crystallise and deposit in soft tissue and joints
what are the main mechanisms for gout development
purine overproduction
increased purine intake
decreased uric acid secretion
purine overproduction
when there is increased cell turnover or lysis of cells leading to release of purines and breakdown to uric acid. Causes include myelo- or lymphoproliferative disorders, psoriasis and use of chemotherapy agents
increase purine intake
several foods and beverages that are rich in purines and increase the risk of developing gout. includes seafood, red meat, alcohol and fructose-rich beverages
decreased uric acid secretion
uric acid is predominantly renally excreted so anything that affects the kidneys can increase the risk of developing gout. Causes include diuretics, acute kidney injury, CKD, ACE inhibitors and diabetes mellitus
crystal formation
high uric acid levels leads to supersaturation and precipitation of monosodium urate crystals in soft tissue, joints and kidneys. Monosodium urate crystals precipitate in peripheral joints because they are less soluble at low temperatures
shape of urate crystals
forms needle-like crystals that can be detected on plane-polarised light. Characteristically monosodium urate crystals are negatively birefringent
symptoms caused by crystal formation
deposition of crystals can occur asymptomatically, such as in chronic gout
acute attacks = crystals trigger an acute inflammatory reaction leading to acutely painful swollen joints
classical presentation of gout
acutely painful and swollen joint coming on abruptly
intensity reached within 12 hours and lasts less than 2 weeks if untreated
joints affected
typically affects first metatarsalphalangeal joint
other common joints:
- knees
- ankles
- wrists
- finger joints
can affect more than 1 joint at a time = polyarticular gout, this is rarer
untreated hyperuricaemia
chronic tophaeous gout
development of multiple tophi - collections of urate crystals in soft tissue
classically located on helix of ear, fingers, toes, prepatellar bursa and olecranon
recurrent flares of acute gout
can lead to chronic polyarticular arthritis
types of gout
acute monoarticular gout
acute polyarticular gout
chronic tophaeous gout
presentation of acute monoarticular gout
joint pain
joint swelling
erythema
most commonly 1st metatarsophalangeal joint
presentation of acute polyarticular gout
joint pain
joint swelling
erythema
fingers, toes, wrists, ankles and knees
presentation of chronic tophaeous gout
tophi
degenerative arthropathy
diagnosis
clinical diagnosis joint aspiration serum uric acid plain radiographs screening for cardiovascular and renal disease
serum uric acid
levels should be taken 4-6 weeks following acute attack
elevated levels are not diagnostic of gout and normal serum uric acid doesn’t exclude gout
during an acute attack, plasma urate levels often fall
joint aspiration
gold standard investigation
often not required
should be completed if there is concern about septic arthritis or where diagnosis is in doubt
send joint fluid for crystal microscopy, microscopy, culture and sensitivities
how is gout diagnosed from microscopy of joint fluid?
presence of needle-shaped monosodium urate crystals that are negatively birefringent under plane-polarised light
plain radiographs
typically normal in acute gout episodes
may show subcorticol cysts or bone erosion
can be used to exclude differentials
management of gout
acute management and long-term prevention
acute management of gout
general advice
first line therapy
second line therapy
general advice for gout
advise rest, ice and elevation of joint
weight loss
diet discussion
alcohol consumption discussed
first-line therapy
NSAIDs - naproxen or oral colchicine
co-prescribe a PPI for gastric protection if giving NSAID
no aspirin!
second-line therapy
if NSAIDs or colchicine are ineffective or contraindicated then give short course of oral steroids or intra-articular injection of steroids
prevention
urate-lowering drugs should be discussed with all patients diagnosed with gout
these drugs should be initiated once an acute attack has resolved
which patient groups should be advised to commence urate-lowering drugs?
2 or more attacks within 12 months tophi chronic gouty arthritis arthropathy renal impairment renal calculi young age onset diuretic use
prevention: first-line therapy
allopurinol
monitor uric acid levels every 4 weeks and dose can be uptitrated in relation to levels
aim for uric acid levels
under 300 micromol/L
cautions for allopurinol
renal impairment
can cause severe, potentially life-threatening hypersensitivity syndrome
allopurinol
xanthine-oxidase inhibitor that prevents conversion of hypoxanthine to xanthine and xanthine to uric acid
prevention: second-line therapy
febuxostate if allopurinol contraindicated
LFTs need to be done prior to and after commencing febuxostat as it can cause acute liver injury
uric acid levels should be monitored every 4 weeks and dose uptitrated in relation to these levels
cautions in febuxostat
renal impairment
hypersensitivity to allopurinol and renal impairment may indicate hypersensitivity to febuxostat
prevention of acute attacks
consider colchicine cover when starting or increasing urate lowering therapies such as allopurinol or febuxostat to prevent acute attacks. This may continue for 6 months
don’t stop urate lowering therapies during acute attacks
