Hyperurecemia/gout

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hyperurecemia

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serum uric acid level that is elevated more than 2 std deviations above the poppulaltion mean

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upper limit of normal

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7mg/dl (uricase mtd)

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gout

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dz that is characterized by recurrent acute attacks of urate crystal-induced arthritis
- incl tophi

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tophi

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deposits of monosodium urate in and around the joints and cartilage and in the kidneys as well as uric acid nephrolithiasis

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serum uric acid level rises

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risk of developing gout inc

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gout pts serum uric acid level

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> 7mg/dl

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uric acid

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end product of purine metabolism

-produced from both dietary and endogenous sources
- formation results from the conversion of adenine and guanine moieties of nucleoproteins and nucleotides

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xanthine oxidase

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catalyzes the rxn that occurs as the final step in the degradation of purines to uric acid

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uric acid via kidneys excretion

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300-600mg/day

2/3's of total uric acid

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uric acid via gi tract excretion

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100-300mg/day

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bodies total uric acid content

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1-1.2g

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daily turnover rate of uric acid content

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600-800mg

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urine ph

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1-5

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poorly soluble free acid

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uric acid

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exists as monosoium urate salt

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uric acid

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primary hyperurecemia and gout

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result fr an innate defect in purine metabolism or uric acid excretion

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hyperurecemia

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result fr uric acid overprodxn, impaired renal clearance of uric acid or combo

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enzymatic defect

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pt's with hyperurecemia and gout

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ex of enzymatic defect

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HGPRT
PRPP

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HGPRT

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hypoxanthine-guanine phosphoribosyltransferase

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PRPP

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phosphoribosyl-1-pyrophosphate

synthetase excess

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classified as overproducers or underexcretors of uric acid

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primary hyperurecemia and gout

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overproducers

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synthesize abnormally large amts of uric acid and excrete excessive amts-more than 800-1000mg daily on an unrestricted diet or more than 600 mg daily on a purine-restricted diet

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underexcretors

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90% of pts

produce normal or nearly normal amts of uric acid but excrete less than 600 mg daily on a purine restricted diet

-slightly inc miscible urate pool

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pathway of uric acid

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glomerulus ->proximal convoluted tubule ->distal tubule

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proximal tubule

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here approx 99% if uric acid is reabsorbed into the bloodstream.

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glomerulus

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uric acid is filtered and enters proximal tubules

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distal tubule

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uric acid is secreted

about 75% of the amt secreted is reabsorbed therefore almost all urinary uric acid is excreted at the distal tubule

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hematological

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assoc with inc nucleic acid turnover and breakdown of uric acid

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hematological causes

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lymphoproliferative disorders
myeloporliferative disorders
hemolytic anemia
hemoglobinopathies

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hyperuricemia

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reduced renal clearance of uric acid

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asa and other salicylates

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inhibit tubular secretion of uric acid at low doses

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uricosuria

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high doses of asa and other salicylates

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inc uric acid conc by enhancing nucleic acid turnover and excretion

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cytotoxic drugs

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ethambutol and nicotinic acid

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inc uric acid conc

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cyclosporine
pyrazinamide
levodopa

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dec renal urate clearance

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ethanol

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alters uric acid metabolism by inc uric acid producxn thru an inc in adenine nucleotide catabolism and by suppressing renal uric acid excretion as a result of lactate inhibition of renal tubular uric acid secretion

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examples of conditions that may cause hyperuricemia

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diabetic ketoacidosis
psoriasis
chronic lead poisoning

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gouty arthritis

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monosodium urate crystals are deposited in the synovium of involved joints

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inflam response to mono-na urate crystals

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leads to an attack of acute gouty arthritis

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sx of acute gouty arthritis

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redness
warmth
tenderness

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tophi or tophaceous deposits

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deposits of monosodium urate crystals

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lead to joint deformity and disability

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untreated gout -> tophi

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kidney involvement

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lead to renal impairment

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renal complications of hyperurecemia & gout

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acute tubular obstruction
urolithiasis
chronic urate nephropathy

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acute tubular obstruction

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develop 2ndary to uric acid preceipitation in the collecting tubules and ureters with subsequent blockage and renal failure

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urate oxidase (rasburicase)

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used in prophylaxis and trmt of hyperurecemia in peds w/ leukemia, lymphoma and solid tumor malignancies who are receiving anticancer therapy

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conversion of uric acid to allantoin

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5x more soluble in urine than uric acid

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urolithiasis

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formation of uric acid stones in the urinary tract

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contributing factor to urolithiasis

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low urine pH

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chronic urate nephropathy

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urate deposits arise in the renal interstitium

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asymptomatic hyperuricemia

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elevated serum uric acid level but has no s/s of deposition dz

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deposition dz

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arthritis
tophi
urolithiasis

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acute gouty arthritis

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painful arthritic attacks

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pathogenesis of acute gouty arthritis

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monosodium salts -> articular tissue ->inflam rxn

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initial attack

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abrupt
night or early am -> synovial fluid reabsorbed

involves a few joints

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most common site of initial attack

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1st metatarsophalangeal joint

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podagra

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attack at metatarsophalangeal joint

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common serum findings for acute gouty arthritis

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leukocytosis
moderately elevated erythrocyte sedimentation rate

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pseudogout

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calcium pyrophosphate dihydrate crystal dz

septic arthritis

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drug trmts

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nsaids
indomethacin
naproxen
sulindac
colchicine
methyprednisolone acetate
prednisone
corticotropin
triamcinolone acetonide

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colchicine

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relieves pain and inflam and ending acute attack

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moa colchicine

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impairs leukocyte migration to inflammed areas and disrupts urate deposition and the subsequent inflam response

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iv colchicine

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shld never be given IM or subcutaneously due to tissue irritation

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bone marrow depression

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colchicine therapy

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intracritical gout

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symptom free period after 1st attack

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inc urate productxn

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high purine diet
obesity
alcohol comsumption

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high purine diet

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all meats
organ meats
seafood
beans
peas
asparagus

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prophylaxis of acute gout attack

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low doses colchicine
low dose nsaids

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urate reducing drug therapy

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uricosurics
xanthine oxidase inhibitor

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uricosurics

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increse renal uric acid excretion

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zanthine oxidase inhibitor

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reduces uric acid production

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probenecid
sulfinpyrazone

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uricosurics

preferred for underexcretors

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long term uricosuric therapy

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reduces teh incidence of gouty arthritis attacks

prevents formation of new tophi

helps resolve existing tophi

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uricosuric moa

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blk uric acid reabsorption at the proximal convoluted tubule -> inc rate of uric acid excretion

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uricosuric indication

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reduce hyperurecemia for pt's excreting less than 600mg of uric acid per day

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not initiated during an acute gout attack

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uricosuric therapy

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maintain high fluid intake

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during uricosuric therapy to dec renal urate precipitation

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greatest potential risk of uricosuric drugs

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-formation of uric acid crystals in urine
-deposition of uric acid in the renal tubules, pelvis or ureter causing renal colic or the deterioration of renal fxn

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maintain an high alkaline irone volume

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take 1 g of sod bicarb 3-4x a day + high intake of fluid -> 2L/day

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c/i

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urinary tract stones

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asa
salicylates

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antagonize axn of uricosurics

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sulfinpyrazone

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reduces platelet adhesiveness
cause bld dyscrasias

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allopurinol moa

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long acting metabolite, oxypurinol, blk the final steps in uric acid synthesis by inhibiting xanthine oxidase

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xanthine oxidase

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enzyme that converts xanthine to uric acid -> reduces serum uric acid level while inc renal excretion of more soluble oxypurine precursors-> dec the risk of uric acid stones and nephropathy

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allopurinol indicaions

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doc for lowering uric acid levels in both underexcretors andoverproducers

preferred urate reducing agt

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se of allopurinol

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exfoliative dermatitis