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GOUT: DIAGNOSIS AND MANAGEMENT

GOUT: DIAGNOSIS AND MANAGEMENT. Gout. Metabolic disorder due to excessive accumulation of uric acid in tissues leading to acute and chronic arthritis and soft tissue and bone deposition of uric acid ( tophi ). Acute Gouty Arthritis. Abrupt onset often at night

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GOUT: DIAGNOSIS AND MANAGEMENT

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  1. GOUT:DIAGNOSIS AND MANAGEMENT

  2. Gout Metabolic disorder due to excessive accumulation of uric acid in tissues leading to acute and chronic arthritis and soft tissue and bone deposition of uric acid (tophi).

  3. Acute Gouty Arthritis • Abrupt onset often at night • 75% of initial attacks in first MTP joint • Usually monoarticular, may be polyarticular • Attack subsides in 3-10 days • Na+ urate crystals in synovial fluid • Hyperuricemia may or may not be present

  4. The victim goes to bed and sleeps in good health. About 2 o’clock in the morning he is awakened by a severe pain in the great toe; more rarely in the heel, ankle or instep.

  5. The pain is like that of a dislocation, and yet the parts feel as if cold water were poured over them…Now it is a violent stretching and tearing of the ligaments – now it is a gnawing pain, and now a pressure and tightening.

  6. So exquisite and lively meanwhile is the feeling of the part affected, that it cannot bear the weight of the bedclothes nor the jar of person walking in the room. The night is spent in torture.- Thomas Sydenham (1624-1689)

  7. QUESTION: Who gets gout?

  8. ANSWER: Individuals with prolonged hyperuricemia

  9. So who gets hyperuricemia?

  10. Hyperuricemia Overproduction (10%) (80 % idiopathic) • Ethanol • HGPRT or G6PD deficiency • PRPP synthetase overactivity • Myeloproliferative disorders • Cytotoxic chemotherapy • Sickle-cell anemia

  11. Hyperuricemia Underexcretion (90%) (80% idiopathic) • Renal insufficiency • Drugs and toxins • Diuretics • Ethanol • Cyclosporine A • Pyrazinamide • Lead nephropathy • Low dose aspirin • Ketosis

  12. So who gets gout? Young and middle-aged men Individuals with hypertension, obesity,renal insufficiency, metabolic syndrome, organ transplants Patients on diuretics Beer drinkers

  13. Who doesn’t get gout? • Women • Unless • Post-menopausal • Renal insufficiency • Chronic diuretic use • Myeloproliferative disorder

  14. The prevalence of gout is increasing Patients with CHF and renal disease are surviving longer Obesity/metabolic syndrome epidemic More organ transplants Less estrogen used Low dose aspirin use

  15. GOUT: DIAGNOSIS • Presentation • Patient demographics • Physical findings • Differentiate from: • Sepsis • RA • Spondyloarthropathy(psoriasis, reactive) • Lyme

  16. GOUT: DIAGNOSIS • Arthrocentesis and crystal identification • Serum uric acid may be misleading and is not a good diagnostic test for acute gout.

  17. TREATMENT OF ACUTE GOUT • NSAIDS • Intra-articular steroids • Prednisone • Colchicine • PO – no fun • IV – be careful (limited availability)

  18. TREATMENT OF RECURRENT GOUT • PO daily low-dose colchicine • Colchicine neuromypathy • Lower serum uric acid level

  19. TREATMENT OF HYPERURICEMIA: INDICATIONS • Repeated or severe acute gout attacks • Patient preference • Tophaceous/erosive gout • Chemotherapy of hematologic malignancies • Nephrolithiasis

  20. Treatment of Hyperuricemia • Decrease uric acid production • Allopurinol • Febuxostat (Uloric) • Uricosuric agents • Probenecid • Sulfinpyrazone

  21. TREATMENT OF HYPERURICEMIA: ALLOPURINOL/FEBUXOSTAT • Marked hyperuricemia • Increased urinary uric acid excretion • Tophaceous or erosive gout • Renal insufficiency • Nephrolithiasis

  22. TREATMENT OF HYPERURICEMIA: URICOSURICS • Low urinary uric acid excretion • Mild renal insufficiency (Probenecid, sulfinpyrazone)

  23. TREATMENT PEARLS • Aspirin makes gout worse. • Allopurinol/febuxostat is a treatment for hyperuricemia and not acute gout. • Giving allopurinol or febuxostat during an acute attack will prolong the attack. • Starting allopurinol/febuxostat may provoke attacks. • Therefore add colchicine for 6-12 mos.

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