Gout.

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GOUT Disease caused by tissue deposition of Monosodium urate crystals as a result of supersatuaration of extra cellular fluid with MSU.
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Presentation transcript:

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 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

Chronic Gout

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