kuliah gouty arthritis.ppt

8/10/2019 Kuliah Gouty Arthritis.ppt

1/56


2/56

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.


3/56

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


4/56

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


5/56

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.


6/56

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


7/56

Serum Urate Level

during a gouty attack, serum urate levels

are normal in about 20% of cases

repeat blood tests eventually detect

hyperuricemia


8/56

Manifestations of Hyperuricemia

subcutaneous tophaceous deposits

urolithiasis

nephrolithiasisrenal diseases involving the tubules,

interstitium, or glomeruli


9/56

OVERPRODUCTION (METABOLIC)(10%)

PRIMARYSECONDARY

RENAL UNDEREXCRETION (90%)PRIMARYSECONDARY

CLASSIFICATION OF HYPERURICEMIA


10/56

OVERPRODUCTION

PRIMARY

1. IDIOPATHIC

2. SPECIFIC ENZYME DEFECTS(


11/56


12/56

SECONDARY

INCREASED NUCLEIC ACID TURNOVER

a. Lymphoproliferative or myeloproliferativedisorders or their chemotherapy

b. Chronic hemolysisc. Psoriasis

OVERPRODUCTION cont.


13/56

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)


14/56

Underexcretion- Filtration

Almost 100% urate is filtered.

Decreased filtration causesincreased serum uric acid such asin:

Renal failure

Volume depletion


15/56

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


16/56

Decreased secretion causes increased

serum uric acid.

Conditions which contribute to this:

Diuretic therapy

Low-dose salicylate therapyLactic acid

Ketoacidosis

Ethanol

Underexcretion- Secretion


17/56

.

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.


18/56

1. Arthritis (Joint

inflammation):rednesswarmth

tendernessswelling

2. Surrounding soft tissue

inflammation


19/56

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


20/56


21/56

Chronic tophaceous gout.

If untreated, monosodium 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.


22/56

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


23/56

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.


24/56


25/56


26/56

What are the typical

laboratory findings in gout?


27/56


28/56


29/56

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.


30/56

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.


31/56

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


32/56

What are the typical radiographicfindings in gout?


33/56

1. Soft tissue swelling during

acute attack.

2. Soft tissue density if tophiare present.

3. Oval bone erosions withoverhanging edge is

classic abnormality.


34/56


35/56


36/56


37/56

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.


38/56

Treatment


39/56

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.


40/56

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.


41/56

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


42/56


Arthritis

The choice of urate-lowering medications:

uricosuric drugs (which promote uric

acid excretion)xanthine oxidase inhibitors (which

inhibit uric acid production).


43/56


Arthritis

uricosuric drug

Probenecid, benzbromazone

inhibits the tubular reabsorption of

filtered and secreted urate, thereby

increasing urate excretion.

T f Ch i G


44/56


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


45/56


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


46/56


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


47/56


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.


48/56

T f T hi


49/56

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


50/56

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

T t t f T hi


51/56

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.


52/56

T t t f T hi


53/56

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


54/56

Treatment of Tophi

non-drug methods

encourage controlled weight loss

avoidance of alcohol, salicylates andfoodwhich may trigger an acute attack


55/56


56/56

kuliah gouty arthritis.ppt

Documents