Gout Presentation

1. GOUT

2. What is Gout?
•Crystal arthritis
•Deposition of uric acid crystals in joints
•Presents with acute monoarticular arthritis in 90 %
of patients.
•Men > Women
•Onset 40-60 years
•Very treatable
•Untreated, may lead to chronic tophaceous gout.

3. History
•Pain, swelling and redness of affected joint
•Pain exacerbated by movement
•May be pyrexial
•Podagra is initial presentation in 50 %
cases.
•Starts abruptly, max intensity within 8-12
hours.
•Resolves spontaneously < 2 weeks

4. Uric Acid Metabolism
Nucleic Acids
Hypoxanthine
Xanthine
Uric Acid
Xanthine Oxidase
Xanthine Oxidase
Excretion by Kidney

5. What goes wrong?
Nucleic Acids
Hypoxanthine
Xanthine
Uric Acid
Xanthine Oxidase
Xanthine Oxidase
Excretion by Kidney
GOUT
Impaired renal
excretion
Increased nucleic
acids

6. Predisposing Factors
•Gender- male > female
•Family History
•Previous attack
•Body size - large > small
•Alcohol
•Diet – purine rich
•Diuretics
•Causes of high cell turnover e.g. psoriasis,
chemotherapy
•Renal insufficiency

7. What happens in the joint?
•Supersaturation leads to urate crystal
deposition within joint.
•Leads to inflammatory response
® Symptoms

8. Investigations
•Joint aspiration - polarising light
microscopy for crystals
•FBC - white cells raised
•ESR - raised
•X-ray - generally normal
•Serum urate
HIGH SERUM URATE DOES NOT NECESSARILY
MEAN THE PATIENT HAS GOUT!

9. Treatment of Acute Attack
•NSAID
•Colchicine
–GI side effects,
–Most effective in 1
st
24 hours
•Corticosteroid
–If NSAID and colchicine contraindicated
AIM- to reduce symptoms

10. Prevention of Further Attacks
•Lifestyle changes – to minimise risk factors
•Drug therapies
–Xanthine oxidase inhibitors e.g. Allopurinol
–Uricosuric agents e.g. Probenecid
•Need to be taken for life
•Can precipitate an acute attack therefore
give together with NSAID or colchicine for
2 months.
AIM - Prophylaxis

11. Site of drug action
Nucleic Acids
Hypoxanthine
Xanthine
Uric Acid
Xanthine Oxidase
Xanthine Oxidase
Excretion by Kidney
Uricosuric agents
e.g. Probenecid
XO inhibitors
e.g. Allopurinol
GOUT

12. Chronic Tophaceous Gout
•If gout untreated
•Other joint involvement
•Formation of tophi- collection of crystals in
soft tissues
•Bone erosion at joints- ‘punched out’
erosions on x-ray.

13. Tophi

14. X-rays

15. Key Points
•Gout is due to deposition of urate crystals in joints
leading to inflammation.
•Diagnosis is by history and polaroid microscopy
of synovial fluid.
•High serum uric acid does NOT mean the patient
has gout.
•Gout is one of the most treatable arthritic
conditions.
•Treat acute attack and then consider prophylaxis
of future episodes.
•If untreated, can develop into chronic tophaceous
gout.

16. Summary
•Many predisposing/risk factors
•Typical history
•Investigations
•Treatment - understanding of uric acid
metabolism
•Chronic tophaceous gout

17. References
•Francis M, 2006. eMedicine - Gout.
http://www.emedicine.com/med/topic924.htm. Accessed 10/2/2007
•Andrew J, Herrick A and Marsh D. Musculoskeletal Medicine and
Surgery. Churchill Livingstone, London 2000.
•Underwood J. General and Systemic Pathology Third Edition.
Churchill Livingstone, 2003