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Gout
What is Gout?
ā€¢ inflammatory arthritis caused by deposition of
monosodium urate crystals in joints.
ā€¢ Peak incidence in the 50s to 60s
ā€¢ Most common in postpubertal males (uric acid rises after
puberty)
ā€¢ Incidence rises in postmenopausal females (uric acid
rises after menopause)
ā€¢ Men > Women
What goes wrong?
ā€¢ increased production (10%) and diminished excretion
(90%) of uric acid
Clinical Presentation
ā€¢ Asymptomatic hyperuricemia
ā€¢ Acute gout
ā€¢ Chronic (tophaceous) gout
ā€¢ Renal disease
Asymptomatic hyperuricemia
ā€¢ More than 75% of individuals remain asymptomatic.
Acute gout
ā€¢ Acute onset of intense joint pain, swelling, erythema, and heat
ā€¢ Fever (systemic manifestation of inflammation) may be present
ā€¢ 50% of patients present with first metatarsophalangeal joint involvement
(podagra)
ā€¢ Gout may also affect the ankles, midfoot, knees,wrists, shoulders, and
hands
ā€¢ Attacks are usually monoarticular or oligoarticular(two to three joints); rarely
polyarticular until late in the disease course
ā€¢ Early attacks are self-limited and will resolve over 3 to 10
days, even without treatment
Chronic (tophaceous) gout
ā€¢ Tophi ā†’ Deposits of monosodium urate crystals in soft
tissue.
ā€¢ After years of recurrent attacks, joints develop
ā€“persistent pain,
ā€“swelling,
ā€“and deformity
Renal disease
ļ£æ
ā€¢ Nephrolithiasis risk 50% with serum uric acid
greater than 13 mg/dL.
Investigations
ā€¢ Joint aspiration - polarising light microscopy for
crystals
ā€¢ Crystals are needle-shaped, negatively birefringent, and
may be intracellular
ā€¢ FBC - white cells raised
ā€¢ ESR - raised
ā€¢ X-ray - generally normal ā†’ Bone erosion at joints-
punched outā€™
ā€¢ Serum urate
ā†“
Treatment of Acute Attack
ā€¢ AIM- to reduce symptoms
ā€¢ NSAID high dose
ā€¢ Colchicine
ā€“ GI side effects,
ā€“ Most effective in 1st 24 hours
ā€¢ Corticosteroid
ā€¢ ā€“ If NSAID and colchicine contraindicated
Prophylaxis
ļ£æ
ā€¢ Lifestyle changes
ā€¢ Low-purine diet,
ā€¢ discontinue aspirin and diuretics,
ā€¢ limit alcohol
ā€¢ Colchicine 0.6 mg once or twice daily reduces or
eliminates attacks in approximately 95% of patients
Uric acidā€“lowering agents
ā€¢ ā€»Do not start uric acidā€“lowering agents during acute
gout or without prophylaxis, as any change in the uric
acid concentration (up or down) may precipitate an acute
gout attack
ā€¢ Uricosuric agents e.g., probenecid .....have limited
usefulness in setting of renal impairment
ā€¢ Xanthine oxidase inhibition (e.g., allopurinol,
ā€¢ febuxostat)
Gout
Gout

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Gout

  • 2. What is Gout? ā€¢ inflammatory arthritis caused by deposition of monosodium urate crystals in joints. ā€¢ Peak incidence in the 50s to 60s ā€¢ Most common in postpubertal males (uric acid rises after puberty) ā€¢ Incidence rises in postmenopausal females (uric acid rises after menopause) ā€¢ Men > Women
  • 3. What goes wrong? ā€¢ increased production (10%) and diminished excretion (90%) of uric acid
  • 4.
  • 5.
  • 6.
  • 7.
  • 8. Clinical Presentation ā€¢ Asymptomatic hyperuricemia ā€¢ Acute gout ā€¢ Chronic (tophaceous) gout ā€¢ Renal disease
  • 9. Asymptomatic hyperuricemia ā€¢ More than 75% of individuals remain asymptomatic.
  • 10. Acute gout ā€¢ Acute onset of intense joint pain, swelling, erythema, and heat ā€¢ Fever (systemic manifestation of inflammation) may be present ā€¢ 50% of patients present with first metatarsophalangeal joint involvement (podagra) ā€¢ Gout may also affect the ankles, midfoot, knees,wrists, shoulders, and hands ā€¢ Attacks are usually monoarticular or oligoarticular(two to three joints); rarely polyarticular until late in the disease course ā€¢ Early attacks are self-limited and will resolve over 3 to 10 days, even without treatment
  • 11. Chronic (tophaceous) gout ā€¢ Tophi ā†’ Deposits of monosodium urate crystals in soft tissue. ā€¢ After years of recurrent attacks, joints develop ā€“persistent pain, ā€“swelling, ā€“and deformity
  • 12. Renal disease ļ£æ ā€¢ Nephrolithiasis risk 50% with serum uric acid greater than 13 mg/dL.
  • 13. Investigations ā€¢ Joint aspiration - polarising light microscopy for crystals ā€¢ Crystals are needle-shaped, negatively birefringent, and may be intracellular ā€¢ FBC - white cells raised ā€¢ ESR - raised ā€¢ X-ray - generally normal ā†’ Bone erosion at joints- punched outā€™ ā€¢ Serum urate ā†“
  • 14.
  • 15.
  • 16. Treatment of Acute Attack ā€¢ AIM- to reduce symptoms ā€¢ NSAID high dose ā€¢ Colchicine ā€“ GI side effects, ā€“ Most effective in 1st 24 hours ā€¢ Corticosteroid ā€¢ ā€“ If NSAID and colchicine contraindicated
  • 17. Prophylaxis ļ£æ ā€¢ Lifestyle changes ā€¢ Low-purine diet, ā€¢ discontinue aspirin and diuretics, ā€¢ limit alcohol ā€¢ Colchicine 0.6 mg once or twice daily reduces or eliminates attacks in approximately 95% of patients
  • 18. Uric acidā€“lowering agents ā€¢ ā€»Do not start uric acidā€“lowering agents during acute gout or without prophylaxis, as any change in the uric acid concentration (up or down) may precipitate an acute gout attack ā€¢ Uricosuric agents e.g., probenecid .....have limited usefulness in setting of renal impairment ā€¢ Xanthine oxidase inhibition (e.g., allopurinol, ā€¢ febuxostat)