Gout medication

collection of disorders that result from deposition of monosodium urate crystals in body tissue

men

hyperuricemia- from diseases or drugs that interfere with secretion of uric acid, can be endocrine disorder, lead poisoning, or high doses of salicylates

under excretors of uric acid.

overproduction is less common and is usually from another disease

men > 6mg/dl

women > 7 mg/dl

painful monoarthropathy of usually metatarsophalangeal joint of great toe.

2nd episode usually within 6 months to 2 years after first attacks.

sodium urate crystals that are deposited in soft tissue occurs in 50% of patients.

• HTN
• thiazide and loop diuretics
• obesity
• alcoholism (moonshine is worse due to lead content) beer and spirits- not wine
• age > 60
• intake of meat and seafood increase the risk

septic joint

-get synovial fluid for WBCs and diff, crystal analysis and gram stain with culture

increase secretion of uric acid

Tubular blocking agents, increase secretion by blocking reabsorption of urate

Increase risk of stones, increase fluids

• and NSAIDs- decreases or stops the inflammatory process.
• unknown but affects leukocyte fx to reduce lactic acid production.

Not an analgesic and has no effect on uric acid metabolism

decreases or stops the inflammatory process.

decrease the synthesis of uric acid

inhibit xanthine oxidase, the enzyme that converts xanthine to uric acid. Reduces uric acid production.

Does not promote uric acid secretion, so level in renal tubules in not increased

Allopurinol, colchicine, and sulfinpyrazone

xanthine oxidase inhibitors- allopurinol or febuxostat

Urocosuric agents probenecid, fenofibrate, or losartan can be added if xanthine oxidase inhibitors are not sufficient to achieve target serum urate levels.  

HLA-B*5801 allele

NSAIDS and glucocorticoids

first line is colchicine (decreases inflammatory response)

2nd line- Uricosuric (increase secretion) if undersecreter, allopurinol (decreases synthesis of uric acid) if over producer

Long term treatment for urate lowering drugs

baseline then every 2-3 months

2-7 mg/dl

2-6 mg/dl

first time- monitor weekly for toxicity (weakness, nausea, vomiting, diarrhea, and anorexia)

Periodic- LFTs and blood counts (every 3-6 months)

Can cause reversible malabsorption of B12

baseline CBC

• Includes Steven Johnson Syndrome, usually present with rash.
• This is life threatening
• occurs rarely and is dose dependent.

Presents with fever, renal failure, and vasculitis, Mortality around 20%

• diminished renal fx and risk of adverse effects increased.
• -begin with lowest dosage
• -monitor renal fx

• have caused death.
• Gastrointestinal toxicity in 80%
• -bone marrow suppression, blood dyscrasias, hepatic necrosis, and seizures most common in elderly.

safety not established for colchicine and sulfinpyrazone.

probenecid

• B- probenecid
• C- colchicine, allopurinol
• C/D- sulfinpyrazone

• educate on triggers, lifestyle, changes and use of various drugs
• -maintain adequate fluid intake
• -take meds with food to prevent GI upset
• -Report and S&S of GI distress
• -Lose weight slowly, to fast can cause gout attack
• -Stress compliance

notify of skin rash, sore throat, fever, unusual bleeding, bruising, tiredness, weakness, numbness, or tingling

• avoid aspirin or other salicylates can cancel drug
• -increase fluid to prevent stones
• -notify if rash develops

• notify if rash, painful urination, blood in urine, irritation of eyes or swelling of lips and mouth.
• -large doses of vitamin C may increase kidney stones
• -take with fluid and food
• may take 6 weeks for optimal benifit

7 mg

colchicine

hepatotoxicity

NSAIDS

colchicine

corticosteroids

allopurinol and colchicine

Uricosuric agent- probenecid

includes Steven Johnson syndrome.  Skin rash is earliest sign of reaction

heart disease, gi, renal and hepatic, and blood dyscrasias