Gout Flashcards
Indomethacin, NSAIDs GOUT class
Acute attacks of gouty arthritis
Control pain
Indomethacin, NSAIDS GOUT Mechanism
Suppress leukocyte recruitment and activation
Indomethacin, NSAIDS GOUT description
DOC = indomethacin
Others NSAIDs are also useful
Indomethacin, NSAIDs Contraindications
**Aspirin (low dose) ->competes with uric acid for secretion at the PT and causes hyperuricemia***
Indomethacin, NSAIDs GOUT AE
Bleeding
Na+ and H2O retention
Renal insufficiency
Colchicine GOUT class
Acute attacks of gouty arthritis
Control pain
Colchicine GOUT mechanism
Suppress leukocyte recruitment and activation
Colchicine GOUT description
- Binds tubulin* -> decrease polymerization -> no microtubules -> decrease mobility of granulocytes
- Disrupts mitotic spindle* blocking cell division
- Inhibits synthesis/release of LT’s*
Colchicine fun fact
GOUT
no longer used due to side effects
Colchicine AE
GOUT
Abdominal pain
Nausea, vomiting
Diarrhea
Chronic -> myopathy, neutropenia, aplastic anemia, and alopecia
Colchicine contraindications
GOUT
Use with caution in patients with hepatic, renal or CV disease
Glucocorticoids GOUT class
Acute attacks of gouty arthritis
Control pain
Glucocorticoids GOUT mechanism
Suppress leukocyte recruitment and activation
Glucocorticoids description
GOUT
Direct injection into a single affected joint when refractory to NSAIDs or colchicine
Anti-inflammatory and immunosuppressive effects
Allopurinol class GOUT
Chronic gout treatment
Normal serum urate
Allopurinol mechanism
GOUT
Purine analog -> inhibits Xanthine oxidase facilitating dissolution of tophi
Allopurinol description
GOUT
Decreases uric acid synthesis
Prevent renal damage during cancer chemotherapy
Initially may increase attacks due to mobilization of tissue stores of uric acid -> coadminister with NSAID or colchicine
Allopurinol AE
GOUT
Hypersensitivity
Skin rash may progress to Steven-Johnson syndrome (toxic epidermal necrolysis)
Allopurinol contraindications
GOUT
If cutaneous rash develops, discontinue use
Reduce doses of 6-MP and azathioprine -> also metabolized by xanthine oxidase
Probenecid, Sulfinpyrazone class GOUT
Chronic gout treatment
Normal serum urate
Probenecid, Sulfinpyrazone mechanism
GOUT
Competes with urate for a transporter blocking reabsorption in the kidney
Probenecid, Sulfinpyrazone description
GOUT
Uricosuric agents -> enhances uric acid excretion
Coadminister with NSAIDs to prevent acute attack early in treatment
Probenecid, Sulfinpyrazone AE
GOUT
Mild GI irritation
Hypersensitivity
Renal stones (increase fluids)
Sulfinpyrazone can also decrease hematopoiesis and inhibit warfarin metabolism
Probenecid, Sulfinpyrazone Contraindications
GOUT
Gouty patients with nephrolithiasis or overproduction
Blood dyscrasia
Rasburicase class GOUT
Chronic gout treatment
Normal serum urate
Rasburicase mechanism
GOUT
Enzyme that oxidizes uric acid to allantoin which is soluble and easily excreted by the kidney
Rasburicase description
GOUT
Enhances uric acid metabolism *
Prevent renal damage during cancer chemotherapy
Recombinant version of Aspergillus uricase
Gout
High levels of uric acid in the blood -> deposition of sodium urate (end product purine metabolism) crystals in tissues -> inflammation
Urate
Filtered, secreted and reabsorbed in the kidney; only 10% filtered urate is excreted -> reabsorption predominates
Gout and chemotherapy
Cancer chemotherapy causes massive lysis of tumor cells -> significant release of nucleotides** -> hyperuricemia -> massive renal injury (part of tumor lysis syndrome)
