Transcript GOUT - OoCities

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-1pyrophosphate 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
Unknown mechanism
 Levodopa
 Theophylline
 Didanosine
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 hyperuricemia 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.
Gout in transplnat
 Patient
usually on Steroids,azathioprine,cyclosporine
 Colchicine and NSAID use potentially toxic
 Allopurinol increase level of azathioprine and toxicity
 Steroids intra-articular ,oral or parentral can be used
 May need adjust or change transplant medications
Chondrocalcinosis