Gout CUE CARDS Flashcards
What is Gout?
> Most common form of inflammatory arthritis
> Associated with the formation and subsequent deposition of urate crystals in the joints and soft tissues of susceptible individuals
> A condition with acute flares that occur typically on a background of increase serum uric acid
What are the Risk Factors of Gout?
> Obesity
Alcohol (any increases risk)
Foods (fructose containing soft drinks, seafood, meat)
Dairy decreases risk
How is gout diagnosed?
> Symptoms: Pain, swelling and tenderness
Tophi (visible deposits) and hyperuricaemia
First episode: aspirate affect joint and analyse joint fluid via microscopy
What is the Management Overview of Acute Attacks?
What is the Management Overview of Prevention of Further Attacks of Gout?
When is Urate Lowering Therapy Recommended?
> Acute attacks: initiate treatment rapidly to reduce inflammation and symptoms
> Prevention of further attacks: treat underlying cause (e.g. diet)
> Urate lowering therapy is recommended if: non-drug therapy ineffective, more than 1 attack in 12 months, chronic kidney disease or tophi present
What is the aim of treatment of acute gout?
What are critical points/issues?
> Aim to control crystal-induced inflammation and pain (urate crystals remain in joint)
> Critical issues: rapid initiation of treatment, achieve adequate dosing, appropriate duration of treatment
What are established risk factors for GI toxicity?
> Advanced age
Hx of complicated ulcer
Concomitant use of corticosteroids
Higher doses of NSAIDs
Concurrent use of >1 NSAIDs, incl. aspirin
Concomitant administration of anticoagulants
What are Strategies for Gastroprotection?
> COX-2 specific and selective NSAIDs (-coxib, -meloxicam) - lower risk of severe GI toxicity
> Concurrent use of PPIs to reduce the likelihood of developing GI ulcers
What are risk factors of Renal Toxicity?
> Reduced renal blood flow (stressed kidneys) due to:
Hypertension, renal and cardiac failure, severe hepatic disease, systemic infection, older age, certain medications (ACEi, diuretics)
What happens when kidneys are under stress?
> When we have stressed kidneys, out body’s response to that is to produce prostaglandins (by COX-2 enzyme)
> This leads to dilation of the afferent arterioles, which maintains out renal blood flow
What happens to platelet aggregation when we give aspirin and NSAID?
> When we give people aspirin, we inhibit platelet aggregation
> But when we knock off COX 2 enzyme, it will have no effect on the platelet aggregation promotion, but it will knock off COX 2 in the blood vessels, which reduces the prostaglandin H2 and I2 and we lose that effect of inhibition of platelet aggregation and the balance gets changed so we get promotion of platelet aggregation
Discuss previous colchicine dosing
> Previously administered every couple of hours until pain relief was obtained or patient experienced diarrhoea
> These treatment courses were initially limited to a maximum of 8mg but then reduced to a limit of 6mg per course
> After each course, patient need 3 day break before they could receive colchicine again (even if pain still there)
> This went out of favour and was replaced by a regiment of 600mcg tds or qid up to a total course of 6mg, after this patient needs to have 3 day break before taking again
What three recent findings have changed how we use allopurinol?
> Maintenance of serum urate <0.36mmol/L reduces the number of gout attacks
> Most individuals dosed according to renal function don’t achieve target serum urate concentrations (ignore R.F. when uptitrating)
> A target of 0.3mmol/L is appropriate in patients with tophi as there patients have a greater load of urate in their body
When is Febuxostat used?
> Inhibitor of xanthine oxidase and PBS listed (restricted) for prevention in gout attacks in patients for whom allopurinol is CI or not tolerated
