Gout Flashcards
What is gout?
Hyperuricaemia. Deposition of monossodium urate monohydrate in joints & self tissue -> acute inflammation & eventually tissue dmg
What is primary gout?
Due to rare inborn errors of metabolism or renal excretion
What is secondary gout?
Occur due to drugs / consequence of other disorders.
What is the pathophysiology of gout?
Physiological pH -> uric acid is ionised -> monosodium urate.
If supersaturation occurs -> crystal formation.
Crystal depositoin may continue for many years wihtout causing symptoms.
Only causes problems when it sheds into the blood into small sacs of synocial fluid -> inflammation
What are the 5 stages of clincal presentation of gout?
Asympotmatic hyperuricaemia
Acute gouty arthritis
Interval gout /Intercritical gout
Chronic tophaceous gout.
Gouty nephropthy
What is Acute gouty arthritis?
Caused by deposition of urate crystals in joints.
Severe pain with hot, red, swollen & extremely paindul joints.
Begin abruptly - max pain 8-12 hrs.
What is intercritical gout?
Time between acute attacks of gout. Variable intervals of months - yrs where there are no symptoms
What is chornic Tophaceous gout?
Presence of tophi:
White deposites of monosodium urate.
Nodule formation affecting joints.
What is gouty nephropathy?
Crystals of gout deposited around renal tubules -> inflammatory response.
Renal stone formation.
How do you diagnose gout?
Based on clicnical histroy & examination
Uric acid lvls can be useful but not always raised when someone has an acute attack.
Joit fluid microscopy - Presense of crystals & absence of infection.
What is the aim for the treatment of gout?
Releive pain / inflammation of acute attack.
Terminate attack.
Prevent further attacks
Prevent long term joint & organ dmg
During an acute attack of gout what would the first line treatment be?
NSAIDs:
Releive pain & Inflammation
Can abort an acute attack if taken early enough
Full therapeutic range - High dose for 24-48hrs then lower doses for 7-10 days.
Consider PPI
During an acute attack of gout what would the second line treatment be?
Colchicine:
Slower onset - High lvls of toxicity.
–| neutrophil migration into joints.
Administer ASAP -> less effective over time.
What is the does of Colchicine in an acute attack?
O.5mg 2-4 / Day until releif of joint pain / development of GI s/e total of 6mg / Day
Do not repeat course within 3 Days
Lower dose of 0.5mg / 8 hrs in elerdly/renal impairment.
What are the S/E of colchicine?
Nausea & Vominiting.
Abdominial pain
Diarrhoea -> stop therapy immediatley.
What dose of CC would you give in acute gout?
Prenisolone 30-35mg daily
- Pred 35mg for 5 days as effective as naproxen 500mg BD for 5 days for flare treatment.
- Pred 30mg daily for 5 days has analgesic effectiveness equivalent to indomethicin.
When should prophylaxis of gout be considered?
Consider when PtT have 2 or more attaks per yr, tophi, chronic gouty arthritis, joint dmg, renal impairment.
What do Urate Lowering Therapy (ULT) do?
Decreases frequency of flare up
Once crystals have dissolved prevents reoccurence.
Reduce size of tophi & number of tophi.
What is the first line prophylaxis of gout ?
Allopurinol:
Controls symptoms
Some imporvement in tophi
Xanthin odixase –|
Colchicine:
First 6 months
0.5-1mg daily to prevent flare ups and to reach target range.
What dose of allopurinol be given for the prophylaxis of gout?
Start at 100mg daily.
Increase every 3-4 weeks accordinly to response to acheive decrease serum urate lvls.
Usual maintanance dose is 300mg daily (100-600mg)
Drug accumulates in renal impairment (50-100mg daily)
What are teh S/E of allopurinol?
Rashes
Hypersensitivity reactions
GI disturbances.
What is an alternative to allopurinol for the prophylaxis of gout?
Febuxostat:
Alternaitve to allopurinol if C/I or intolerant.
What is the dose of febuxostat?
80mg OD (Increase to 120mg if uric acid lvls >357nmol/L after 2-4 weeks)
What are the S/E of febuxostat?
GI
Headache
Increased LFG
Oedema
Rash
What is the second line treatment for prophylaxis of gout?
Uricosuric Agents: Sulfinpyrazone, probenacid
Avoid urate nephropathy
Ineffective in poor renal function
Need to maintain high fluid intake to reduce risk of store function.
Interactions of Allopurinol and azathioprin?
Azathioprine metabolised into mercaptopurine.
Mercaptopurine metabolised by xanthine oxidase
Allopurinol causes accumulation -> fatal bone marrow suppression.
