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Gout. Gout. Deposits of sodium urate crystals in articular, periarticular, and subcutaneous tissues May be primary or secondary Primary – hereditary error of purine metabolism Secondary – drugs that inhibit uric acid excretion or another acquired disorder. Incidence and Risk Factors.
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Gout • Deposits of sodium urate crystals in articular, periarticular, and subcutaneous tissues • May be primary or secondary • Primary – hereditary error of purine metabolism • Secondary – drugs that inhibit uric acid excretion or another acquired disorder
Incidence and Risk Factors • Primary gout accounts for 90% of cases • Affects primarily middle aged men • Risk factors: obesity, HTN, thiazide diuretics, excess alcohol use
Pathophysiology • Uric acid is end product of purine metabolism and is excreted by the kidneys • Hyperuricemia results from • Increase in uric acid production • Underexcretion of uric acid by kidneys • Both • Diet high in purines will not cause gout, but may trigger an attack in a susceptible person
Clinical Manifestations • Gouty arthritis in one or more joints (but less than four • Great toe joint most common first manifestation; other joints may be the foot, ankle, knee, or wrist • Joints are tender & cyanotic • May be precipitated by trauma, surgery, alcohol ingestion, or infection
Clinical Manifestations • Onset usually nocturnal, with sudden swelling and excruciating pain • May have low grade fever • Usually subsides within 2-10 days • Joints are normal, with no symptoms between attacks
Complications • Joint deformity • Osteoarthritis • Tophi may produce draining sinuses that may become infected • Renal stones, pyelonephritis, obstructive renal disease
Diagnosis • History & physical examination • Family history of gout • Diagnostic studies
Diagnostic Studies • Serum uric acid levels > 6 mg/dl • May be caused by other factors • 24 hour urine uric acid levels • Synovial fluid aspiration contains uric acid crystals • Seldom necessary, as diagnosis based on clinical symptoms possible in 80% of cases • X-rays appear normal in early stages; tophi appear as eroded areas of bone
Collaborative Care • Acute attack • Colchicine produces dramatic antiiflammatory effects with relief within 24-48 hours • NSAIDs for additional pain relief • Corticosteroids (po or intraarticular) • Adrenocorticotropic hormone (ACTH) • Joint aspiration to decompress
Collaborative Care • Prevention of acute attacks • Colchicine combined with: • allopurinol (Zyloprim, Alloprim) – blocks production of uric acid • probenecid (Benemid), sulfinpyrazone (Anturane) – inhibit tubular reabsorption of uric acid • febuxostat (Uloric) – inhibits xanthine oxidase, recently shown to reduce serum uric acid levels
Collaborative Care • Dietary measures • Weight reduction • Avoidance of alcohol • Avoidance of foods high in purines • High: Sardines, anchovies, herring, mussels, liver, kidney, goose, venison, meat soups, sweetbreads, beer & wine • Moderate: Chicken, salmon, crab, veal, mutton, bacon, pork, beef, ham
Collaborative Care • Prevention of renal stones • Increase fluid intake to maintain adequate urine output • Allopurinol • ACE inhibitor losartin (Cozar) – promotes urate diuresis
Nursing Care • Acute gouty arthritis – pain control • Gentle, supportive care of affected joints • Immobilize and rest affected joints – bed rest or NWB • Cradle or footboard to prevent pressure from bedcovers • Monitor ROM and degree of pain
Nursing Care • Patient/Family teaching • Gout is a chronic disease • Drug teaching • Need to monitor serum uric acid levels • Precipitating factors • Excess calorie intake, alcohol intake, purine rich foods • Fasting • Niacin, ASA, diuretics • Surgery or major medical event such as MI