Gout Flashcards
DDx of acute monoarthritis?
Crystal arthropathy
- gout - urate deposition
- pseudogout (calcium pyrophosphate deposition)
- calcium oxalate crystal deposition
Septic arthritis
- gonoccocal (associated sx include tenosynovitis, a new rash, uretheral discharge)
- non gonoccocal (staph aureus, hx of IVDU, prosthetic joint, joint surgery, immunosuppression)
Osteoarthritis (typically milder sx)
Rheumatoid arthritis (rarely presents as a monoarthritis) Psoriatic arthritis, reactive artheritis, Enteropathic arthritis acn cause inflammatory bowel disease
(ref Bones and Joints Check 2015)
How do you differentiate between septic joint and gout?
Crystal arthropathy can present in an identical manner to gout.
Cannot reliably distinguish with clinical presetation, WCC, ESR/CRP or synovial WCC counts.
If high suspicion of septic arthritis - joint aspiration and IV
If aspirate is negative for culture - not septic joint
Looking for urate crystals
(ref Bones and Joints Check 2015)
What causes gout?
Hyperurecemia -> deposition in joints -> inflammatory reaction = gout → subclinical chronic syndovitis / bone erosion and cartilage loss
(ref: NPS article 2004, mangement of acute gout, Dr Neil McGill)
How does gout present?
1/ Acute onset, nocturnal pain with swelling and erythema and loss of function.
> 1st episode 60% have 1st MTP involvement
Can present in elbows, wrist, carpal and tarsal joints, ankles and knees (e.g. olecranon bursitis)
Elderly patients can present as a poly-articular disease
Is there a difference in how it presents in men vs women?
Men tend to be mono articular, females tend to present poly-articular presentation.
How do you differentiate between septic joint and gout?
Crystal arthropathy can present in an identical manner to gout.
>Cannot reliably distinguish with clinical presentation, WCC, ESR/CRP or synovial WCC counts.
>If high suspicion of septic arthritis - joint aspiration then IV abx.
>If aspirate is negative for culture - not septic joint
→ for gram stain, culture and synovial fluid examination, crystals
(ref: NPS article 2004, mangement of acute gout, Dr Neil McGill)
Treatment of acute gout:
1/ NSAIDs or COX-2 inhibitors for the duration of the attack and for one further week after
2/ Colchicine 1mg as soon as possible, then 500micrograms one hour later (don’t repeat within three days)
3/ Oral prednisolone 15-30mg for 3-5/7
(ref: NPS article 2016, management of acute gout)
Definition of hyperurecemia in
1/men 2/women?
Hyperuricaemia is defined as a serum uric acid
more than 0.42 mmol/L in men.
more than 0.36 mmol/L in women
What is the urate target for patients?
Without tophi <0.36mmo/L
With toph <0.30mmol/L
What % of patients with hyperurecemia develop gout? Is there evidence to decrease uric acid levels in asymptomatic patients?
10%
Nil evidence of urate lowering therapy in asymptomatic patients
Which conditions can precipitate gout?
IHD, HT, CKD - independent risk factors for gout
(ref etg)
Obesity - Increase insulin in obese patients inhibits the secretion of uric acid (ref etg)
When patient is on urate lowering therapy, prophylaxis should be used for 6 months to prevent flares of gout.
1/ Colchicine 500micrograms BD (normal renal function) 500micrograms daily (renal impairment)
OR
2/ Prednisolone 5mg daily (etg)
What is colchicine and what’s its MOA?
Xanthine → hypoxanthine → uric acid
(xanthise oxidase catalyses both of these reactions)
Colchicine is a xanthine oxidase inhibitor
(ref: NPS article 2016, management of acute gout)
What is the MOA of allopurinol?
Allopurinol purine analogue competitively inhibits xanthine oxidase (reduces the production of uric acid)
How do you start allopurinol?
1/ In patients with normal renal function, allopurinol should be started at a dose of 100 mg daily for the first month.
2/Increase the daily dose by 50 mg every 2–4 weeks until the target serum uric acid concentration is reached.
3/Plasma urate concentrations can be measured monthly during this tit-ration phase and doses higher than 300 mg daily are often required to reach the target
Maintenance, oral, usually 300–600 mg (maximum 900 mg) daily, irrespective of renal function (Ref AMH).
(ref: NPS article 2016, management of acute gout)