kuliah gouty arthritis.ppt
TRANSCRIPT
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DEFINITION OF GOUT
An acute arthritis caused by the
inflammatory response to
monosodium urate crystals in thejoint.
Neutrophils phagocytose the crystalsand degranulate. The enzymes
released cause the clinical
manifestations of inflammation.
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Epidemiology
men women
mean age of onset 49 60
incidence (age 32-64) 2.8% 1.5%
the lower incidence and later onset of gout in women
is attributed to more efficient urate excretion
attack before the age of 30 is rare and suggest a
genetic metabolic disorder
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Pathophysiology
Gout is caused by disorders ofpurine
metabolismresulting in elevated levels of
uric acid
> 7 mg/dl in men
> 6 mg/dl in women
prolonged hyperuricemia leads to
formation of monosodium urate
monohydrate crystals
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The 4 stages of gout
Asymptomatic hyperuricemic (but manyhyperuricemic people do not developgout)
Acute gouty arthritis (the usualpresentation)
Intercritical gout (variable symptom-freeperiods between acute attacks may last
weeks or years)Chronic tophaceous gout.
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Serum Urate Level
any sudden change in serum urate
concentration can provoke an acute gouty
attack
sudden increasefavors formation of new
crystals
sudden decreasepromotes shedding of
previously formed crystals from the synovialmembrane
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Serum Urate Level
during a gouty attack, serum urate levels
are normal in about 20% of cases
repeat blood tests eventually detect
hyperuricemia
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Manifestations of Hyperuricemia
subcutaneous tophaceous deposits
urolithiasis
nephrolithiasisrenal diseases involving the tubules,
interstitium, or glomeruli
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OVERPRODUCTION (METABOLIC)(10%)
PRIMARYSECONDARY
RENAL UNDEREXCRETION (90%)PRIMARYSECONDARY
CLASSIFICATION OF HYPERURICEMIA
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OVERPRODUCTION
PRIMARY
1. IDIOPATHIC
2. SPECIFIC ENZYME DEFECTS(
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SECONDARY
INCREASED NUCLEIC ACID TURNOVER
a. Lymphoproliferative or myeloproliferativedisorders or their chemotherapy
b. Chronic hemolysisc. Psoriasis
OVERPRODUCTION cont.
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PRIMARY
1. Idiopathic
SECONDARY
1. Acute or chronic renal failure
2. Volume depletion3. Altered renal tubular handling of uric
acid due to drugs, volume status or
endogenous metabolic products
A. Filtration
B. Reabsorption
C. Secretion
Underexcretion (Renal Handling of urate)
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Underexcretion- Filtration
Almost 100% urate is filtered.
Decreased filtration causesincreased serum uric acid such asin:
Renal failure
Volume depletion
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Increased reabsorption causes increasedserum uric acid as in:
Volume depletion
Decreased reabsorption causes decreaseduric acid = uricosuria.
Medications which cause uricosuria are: Probenecid
SulfinpyrazoneHigh-dose salicylate
Underexcretion- Reabsorption
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Decreased secretion causes increased
serum uric acid.
Conditions which contribute to this:
Diuretic therapy
Low-dose salicylate therapyLactic acid
Ketoacidosis
Ethanol
Underexcretion- Secretion
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.
Acute gouty arthritis.
Acute onset of severely painful arthritis usually
in lower extremities. Often early attacks in 1st
MTP joint (podagra). May be precipitated by
trauma, surgery or major medical illness,
alcohol ingestion, or systemic infections. Initial
attacks self-limited but may become chronic.Synovial fluid is inflammatory with needle-
shaped monosodium urate crystals with strong
negative birefringence.
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1. Arthritis (Joint
inflammation):rednesswarmth
tendernessswelling
2. Surrounding soft tissue
inflammation
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Gouty arthritisresults from deposition of sodium urate crystalsinjoints. The joint most often affected is the first MP joint (big toe) as
seen here. Acute attacks are characterized by severe pain, swelling,
and erythema of the joint.
Source: WebPath
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Chronic tophaceous gout.
If untreated, mono- sodium urate maydeposit in cartilage, tendons, bursae, softtissue and synovium in deposits calledtophi. These are commonly found inolecranon bursae, Achilles tendon, around
joints and ear. May extrude white pasty
material and can limit joint mobility.
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Chronic tophaceous gout
persistent gout chronic tophaceousgout produces toph i,
solid deposits of of monosodium urate
crystals
form in the joints, cartilage, bones,
and elsewhere in the body.
develop on average about 10 years
after the onset
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Gouty tophi project from the fingers as rubbery nodules. Below:
A section from a tophus shows extracellular masses of uratecrystals with accompanying foreign body giant cells.
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What are the typical
laboratory findings in gout?
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1. Inflammatory synovial fluid
a. Cloudyb. 20,000 to 100, 000 WBC/mmc. Predominately PMN
2. Monosodium urate crystals in synovial fluida. Needle-shaped
b. Strong, negative birefringence withcompensated polarized light
3. Serum uric acid is elevated at some time in almostall patients. However it is NOT
DIAGNOSTIC.
4. Urine uric acid >750 to 1000 mg/day suggestsoverproduction of uric acid.
5. May have leukocytosis, high ESR, increased C-reactive protein during acute attack.
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If synovial fluid is aspirated from a patient with gout, thefluid can be examined for
the presence of sodium urate crystals, which are seen here
to be needle shaped.
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Differential Diagnosis
Septic Arthritis
Septic and gouty arthritis present with
many of the same signs and symptoms
fever and monoarthritis
Beware: both septic and gouty arthritis
may present in the same joint
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What are the typical radiographicfindings in gout?
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1. Soft tissue swelling during
acute attack.
2. Soft tissue density if tophiare present.
3. Oval bone erosions withoverhanging edge is
classic abnormality.
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Chronic gout leads to deposion of urates into a chalky mass known
as a "tophus". Such tophi can destroy the joint and adjacent bone asseen in these sequential radiographs of the same foot.
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Treatment
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Acute Gout
(1) Nonsteroidal antiinflammatory drugs
(2) Corticosteroids if resistant to NSAID
and colchicine, of if they are contraindicated
(3) Colchicinegenerally outmoded foracute attack. Often used as maintenance
antiinflammatory agent
(4)Allopurinol and uricosuric drugs are of
no benefit in acute gout and may make acuteattack more difficult to control.
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Treatment of Acute gouty arthritis
Colchicine-- inhibits neutrophil activation,effective, less frequently because of its side
effects.
Colchicine -- 0.5-mg dose every hour until :
improvement, GI adverse effects (abdominalpain, diarrhea, and nausea), or a total of 10
doses without relief.
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Treatment of Acute gouty arthritis
Indomethacin and other NSAID -- drugs ofchoice
NSAIDs -a 7-10 day course or until 3-4 daysafter all signs of inflammation have resolved.
Use NSAIDs with caution -- in edematousstates, such as heart failure, peptic ulcerdisease or renal insufficiency.
Treatment of Chronic Gouty
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Treatment of Chronic Gouty
Arthritis
The choice of urate-lowering medications:
uricosuric drugs (which promote uric
acid excretion)xanthine oxidase inhibitors (which
inhibit uric acid production).
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Treatment of Chronic Gouty
Arthritis
uricosuric drug
Probenecid, benzbromazone
inhibits the tubular reabsorption of
filtered and secreted urate, thereby
increasing urate excretion.
T f Ch i G
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Treatment of Chronic Gouty
Arthritis
Allopurinol is competitive inhibitorsof
the enzyme xanthine oxidase
Treatment principle: lower the plasma
urate concentrationto such a degree, as
to allow urate to be resorbed from the
surface of the tophi.
T f Ch i G
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Treatment of Chronic Gouty
Arthritis
The ideal candidates for allopurinol treatment
are
uric acid overproducersrenal insufficiency
nephrolithiasis
tophaceous goutat risk for developing uric acid nephropathy
T f Ch i G
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Treatment of Chronic Gouty
Arthritis
allopurinol can be used in almost any
hyperuricemic state
the usual maintenance dose for adults is
between 200 and 300 mg/d
long half-life of oxypurinol makes once
daily dosingpossible.
T t t f Ch i G t
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Treatment of Chronic Gouty
Arthritis
skin rash may proceed into severehypersensitivity reactions
patients who develop a skin rash shoulddiscontinue allopurinol.
hepatotoxicity, bone marrow depression,and interstitial nephritis are rare butserious adverse effects of allopurinol.
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T f T hi
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Treatment of Tophi
al lopur inolis the treatment of choice.dose of al lopur inol serum uric acid
response checked after 3 months
adjust the dose(al lopur inol
300mgtablet)
treatment will be life-long
at the start of therapy acute attacks mayoccur
T t t f T hi
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Treatment of Tophi
The concomittant use of a NSAIDor aprophylactic dose of colch ic inefor thefirst month of treatment with al lopur inolis therefore recommended
al lopur inolshould likewise not bestarted within 1 month of an acuteattack of gout, as it may precipitate
another attack
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Treatment of Tophi
The activity of allopurinolanduricosuricsis additive
when administered concomitantly,
smaller dosesof each drug can be usedCombined use of the 2 types of drugs isespecially effective in the presence oftophaceous deposits.
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T t t f T hi
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Treatment of Tophi
Surgeryis rarely used to treat gout.
Surgical indication: draining, infected,
or are interfering with the movement of
your joints
It is sometimes necessary to replace
joints.
T t t f T hi
http://www.orthop.washington.edu/arthritis/living/surgeryhttp://www.orthop.washington.edu/arthritis/living/surgery -
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Treatment of Tophi
non-drug methods
encourage controlled weight loss
avoidance of alcohol, salicylates andfoodwhich may trigger an acute attack
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