Your Federal Quarterly Tax Payments are due April 15th Get Help Now >>

Stages of Gout Prolonged a symptomatic hyperuricemia years Acute intermittent Gout Chronic tophaceous Gout GOUT by WJQQY8G

VIEWS: 0 PAGES: 33

									                 GOUT
Disease caused by tissue deposition of
Monosodium urate crystals as a result
of supersatuaration of extra cellular fluid
with MSU.
               Hyperuricemia
 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 Hyperuricemia
PURINES DEGREDATION PRODUCT

OVERPRODUCTION OF URATE
ENDOGENOUS OR EXOGENOUS
UNDEREXCRETION OF URATE (RENAL)
90% OF GOUT PATIENT
COMBINATION OF THE ABOVE TWO
              EPIDEMIOLOGY
Disease of adult men with peak in 5th decade.
Very rare before puberty and in premenopausal
 women.
Less than 25% of hyperuricemic develop GOUT
Duration and serum uric acid directly correlate
 with Gout development
20% family history
                      Primary
 Under  excretion:
 Idiopathic 90% of patients
  with hyperuricemia.
Normal excretion of uric
  acid only when serum uric
  acid high
         Over production :rare
Idiopathic
Hypoxanthine-guanine phosphoribosyltransferase
 deficiency
Phosphoribosyl-1-pyrophosphate synthetase
 super activity.
         ACQUIRED CAUSES OF
          HYEPERURICEMIA
URATE OVERPRODUCTION
Excess dietary purine consumption
Accelerated ATP degradation : alcohol
 abuse,glycogen storage disease,
Myeloproliferative and Lymphoproliferative
 disorders both causing increased nucleotide
 turnover.
         ACQUIRED CAUSES OF
          HYEPERURICEMIA
Urate under excretion
Renal disease
Poly cystic kidney disease
Hyperparathyroidism
Hypothyroidism
Hypertension
   DRUGS CAUSE HYPERURICEMIA
                      DERCREASED RENAL EXCRETION



Decreased renal excretion
 Cyclosporine
 Alcohol
 Nicotinic acid
 Thiazide
 Lasix(furosemide)
 Ethambutol
 Aspirin (low dose)
 Pyrazinamdie
       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 Gout
Prolonged a symptomatic hyperuricemia(years)
Acute intermittent Gout
Chronic tophaceous Gout
 GOUT: CLINICAL MANIFESATATION
Recurrent Gouty Arthritis( articular and
 periarticular.
Tophi
Uric acid urinary calculi
Interstitial nephropathy with renal function
 impairment
Gout involving DIPs
      Podegra (gout of 1st MTP)
         Gout of ankle joint
Acute onset
Gout affect 1st   MTP 75%
Severe pain
Erythema
Very tender
May be febrile
Resolve 3-10 days
Tophacous Gout
Tophi hands and olecranon
          bursa
Olecranon bursitis
               Gout crystals
Needle like
Can be Intra or extra cellular
Negatively birefringent
                        Gout
Soft tissue swelling   because
of Tophi
Large erosions involving
DIPs,with hanging edges
                        Gout
Soft tissue swelling   around
1st MTP
Erosion around 1st MTP
This takes time to develop
(YEARS)
        Deferential Diagnosis
Pseudo Gout     (CPPD)
Septic arthritis
Reactive arthritis
Other inflammatory arthritis
   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 toxicities
Know NSAIDs contraindications,
          CONTINUE ACUTE GOUT
              MANAGMENT
 Colchicine: 0.6-1mg bid oral
 Limited because of toxicity
 Main side effects GI :abdominal pain/diarrhea/nausea
 Need adjustment in renal impairment
 May cause myelosuppression
 May be linked to azospermia and infertility
 IV Colchicine very toxic to bone marrow
             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.
            Prophylaxis
   Till Acute episode controlled
May use Colchicine
NSAID
     Prevention and control of
    hyperuricemia indications
1-recurrent attacks of Gout
2-renal stones
3-tophaceous Gout
4-chronic gout with joint damage and erosions
5-hyperuricemia uric acid > 12mg/dl
6-24 hr urine excretion of >1100 mg uric acid
         Uricosuric agents
      Probencid,sulfinprazone
Who is  good candidate
1-age <60
2-Creatinine clearance >50ml/min
3-24 hr urine of uric acid < 700mg(under
 excretion)
4-No history of renal stone
     Xanthine oxidase inhibitor
            Allopurinol
Hyperuricemia with :
Urinary uric acid >1000mg
Uric acid nephropathy
Nephrolithiasis
Before chemotherapy
Renal insufficiency GFR<50
Allergy to Uricosuric agents
                    Allopurinol
 Average   dose 300mg
 Renal impairment use lower dose
 May 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.

								
To top