GOUT Disease caused by tissue deposition of Monosodium urate crystals as a result of...
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Transcript of GOUT Disease caused by tissue deposition of Monosodium urate crystals as a result of...
GOUTGOUTDisease caused by tissue deposition of Monosodium urate crystals as a result of supersatuaration of extra cellular fluid with MSU.
HyperuricemiaHyperuricemia
Serum uric acid above normal level for age and sex.
>7mg for adult men and > 6mg for adult women. Only 15-20% of all patient with hyperuricemia
develop gout.Why we produce uric acid :End product of purine
metabolism but human do not have enzyme uricase to convert it to allantoin (highly soluble)
Mechanism of HyperuricemiaMechanism of Hyperuricemia
PURINES DEGREDATION PRODUCT
OVERPRODUCTION OF URATEENDOGENOUS OR EXOGENOUS
UNDEREXCRETION OF URATE (RENAL) 90% OF GOUT PATIENT
COMBINATION OF THE ABOVE TWO
EPIDEMIOLOGYEPIDEMIOLOGY
Disease of adult men with peak in 5th decade.Very rare before puberty and in premenopausal
women.Less than 25% of hyperuricemic develop GOUTDuration and serum uric acid directly correlate
with Gout development20% family history
PrimaryPrimary
Under excretion:Idiopathic 90% of patients
with hyperuricemia.Normal excretion of uric
acid only when serum uric acid high
Over production :rareIdiopathicHypoxanthine-guanine
phosphoribosyltransferase deficiency
Phosphoribosyl-1-pyrophosphate synthetase super activity.
ACQUIRED CAUSES OF HYEPERURICEMIA
ACQUIRED CAUSES OF HYEPERURICEMIA
URATE OVERPRODUCTIONExcess dietary purine consumptionAccelerated ATP degradation : alcohol
abuse,glycogen storage disease,Myeloproliferative and Lymphoproliferative
disorders both causing increased nucleotide turnover.
ACQUIRED CAUSES OF HYEPERURICEMIA
ACQUIRED CAUSES OF HYEPERURICEMIA
Urate under excretionRenal diseasePoly cystic kidney diseaseHyperparathyroidismHypothyroidismHypertension
DRUGS CAUSE HYPERURICEMIA
DERCREASED RENAL EXCRETION
DRUGS CAUSE HYPERURICEMIA
DERCREASED RENAL EXCRETION
Decreased renal excretionCyclosporineAlcoholNicotinic acidThiazideLasix(furosemide)EthambutolAspirin (low dose)Pyrazinamdie
Unknown mechanismLevodopaTheophyllineDidanosine
ALCOHOL MECHANISM OF HYPERURICEMIA
ALCOHOL MECHANISM OF HYPERURICEMIA
Increases lactic acid production which reduces renal excretion of urate.
Increases Urate synthesis because of increased ATP degradation.
Beer also contain purine guanosine.
Stages of GoutStages of GoutProlonged a symptomatic hyperuricemia(years)Acute intermittent GoutChronic tophaceous Gout
GOUT: CLINICAL MANIFESATATIONGOUT: CLINICAL
MANIFESATATIONRecurrent Gouty Arthritis( articular and
periarticular.TophiUric acid urinary calculiInterstitial nephropathy with renal function
impairment
Gout involving DIPsGout involving DIPs
Podegra (gout of 1st MTP)Gout of ankle joint
Podegra (gout of 1st MTP)Gout of ankle joint
Acute onsetGout affect 1st MTP 75% Severe painErythemaVery tenderMay be febrileResolve 3-10 days
Tophacous GoutTophacous Gout
Tophi hands and olecranon bursaTophi hands and olecranon bursa
Olecranon bursitisOlecranon bursitis
Gout crystalsGout crystals
Needle likeCan be Intra or extra cellularNegatively birefringent
Gout Gout
Soft tissue swelling because of TophiLarge erosions involving DIPs,with hanging edges
GoutGout
Soft tissue swelling around 1st MTPErosion around 1st MTPThis takes time to develop(YEARS)
Deferential DiagnosisDeferential Diagnosis
Pseudo Gout (CPPD)Septic arthritisReactive arthritisOther inflammatory arthritis
MANAGEMENT OF ACUTE GOUT
MANAGEMENT OF ACUTE GOUT
NSAID:indomethacin used more than other NSAIDs my use any other NSAIDs at full dose like ibuprofen 800mg TID or Naprosyn 500mg bid expect to as effective as indomethacin and my be less toxic
Know NSAID toxicitiesKnow NSAIDs contraindications,
CONTINUE ACUTE GOUT MANAGMENT
CONTINUE ACUTE GOUT MANAGMENT
Colchicine: 0.6-1mg bid oralLimited because of toxicityMain side effects GI :abdominal pain/diarrhea/nauseaNeed adjustment in renal impairmentMay cause myelosuppressionMay be linked to azospermia and infertilityIV Colchicine very toxic to bone marrow
CONTINUE ACUTE GOUT MANAGEMENT
CONTINUE ACUTE GOUT MANAGEMENT
Steroids safe for acute management with fast results,and when NSAID and Colchicine use not warranted
Intra-articular injection of triamcinolone is fastest way to get relief ,at the same time can get synovial fluid for analysis
Oral or parentral steroids e.g.:prednisolone oral 20-40 mg daily for 5-7 days ,equivalent doses of IV steroids may be used if unable to take oral
Always make sure no infection coexist.
ProphylaxisTill hyperuricemia
controlled
ProphylaxisTill hyperuricemia
controlledMay use ColchicineNSAID
Prevention and control of hyperuricemia indicationsPrevention and control of hyperuricemia indications
1-recurrent attacks of Gout 2-renal stones3-tophaceous Gout4-chronic gout with joint damage and erosions5-hyperuricemia uric acid > 12mg/dl6-24 hr urine excretion of >1100 mg uric acid
Uricosuric agentsProbencid,sulfinprazone
Uricosuric agentsProbencid,sulfinprazone
Who is good candidate1-age <602-Creatinine clearance >50ml/min3-24 hr urine of uric acid < 700mg(under
excretion)4-No history of renal stone
Xanthine oxidase inhibitorAllopurinol
Xanthine oxidase inhibitorAllopurinol
Hyperuricemia with :Urinary uric acid >1000mgUric acid nephropathy NephrolithiasisBefore chemotherapyRenal insufficiency GFR<50Allergy to Uricosuric agents
AllopurinolAllopurinol
Average dose 300mgRenal impairment use lower doseMay precipitate acute gout when first used Side effects can be very serious range from
dyspepsia,headache,diarrhea,rash,to more severe including fever,esosinophilia,interstitial nephritis,hepatitis,vasculitis,acute renal failure,toxic epidermal necrolysis,and hypersensitivity syndrome.
Gout in transplnatGout in transplnat
Patient usually on Steroids,azathioprine,cyclosporineColchicine and NSAID use potentially toxicAllopurinol increase level of azathioprine and toxicity Steroids intra-articular ,oral or parentral can be used May need adjust or change transplant medications
ChondrocalcinosisChondrocalcinosis