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Gout
Gout is a metabolic disorder because
of hyperuricaemia
Person who suffers from gout either
Produces excessive amounts of uric acid
(overproducers)
Unable to excrete its normally
(underexcretors)
RNA, DNA
Purines
Hypoxanthi
ne
Xanthine
oxidase
Xanthine
Uric acid
Pathophysiology of gout
Uric acid reacts with sodium to form
sodium urate
Sodium urate crystals precipitates in
synovial fluid
Irritates the cartilage and triggers
the inflammation
Infiltration of granulocytes
Phagocytosis of urate crystals
Generation of free radicals and
damages the tissues
Release of glycoprotein (proteolytic
enzyme)
Release of lysosomal enzymes and
more joint destruction
Acute gout
Painful arthritic attack of sudden
onset
Usually occur at night or in early
morning
Metatarso-phalangeal joint is
commonly involved
Chronic gout
Large subcutaneous tophi in the
pinna of external ear, eyelids, nose
and around joints
Chronic gout
Large subcutaneous tophi in the
pinna of external ear, eyelids, nose
and around joints
Can lead to joint deformities
Urate crystals in kidney can cause
renal disease
Classification
Uricosuric drugs
Probenecid
Sulfinpyrazone
Benzbromarone
Colchicine
Suppresses gouty inflammatory
response
MoA
It prevents granulocyte migration
into inflamed joint by
binding to intracellular protein tubulin
and
causes depolymerizaton &
disappearance of microtubules in
granulocyte
Adverse effects
Diarrhea
Abdominal pain
Indications
For terminating acute attacks of gout
1 mg orally f/b 0.5 mg every 3 hrs
Until
Pain is relieved or
Diarrhea occurs
NSAIDs
MoA
Inhibit urate crystal phagocytosis &
Chemotactic migration of leukocytes in
to the inflamed joint
Indomethacin is preferred
Better tolerated than colchicine
50 mg every 6 hrly f/b 25 mg 8 hrly for 5
days
Corticosteroids
Reserved drug
Not responding or tolerating to
NSAIDs or colchicine
Intra-articular injection of soluble
steroid is preferred over crystalline
preparations
Systemic steroids requires larger
doses
Allopurinol
Inhibits formation of uric acid by
inhibiting the enzyme xanthine
oxidase
Shorter acting and competitive
inhibitor
Active metabolite (alloxanthine)
Longer acting
Noncompetitive inhibitor
No analgesic
No anti-inflammatory
Ineffective in treatment of acute gout
Indications:
Chronic gout pts with gouty tophi or
nephropathy
Pts with 24 hr urinary uric acid
excretion > 1.1 g
Recurrent renal urate stones
Secondary hyperuricaemia due to
radiotherapy & chemotherapy
Adverse effects
Acute attack of gouty arthritis
Rapid lowering of plasma urate causes
dissolution of tophi
Hypersensitivity reactions
GIT distress
Febuxostat
Patient intolerant to allopurinol
Probenecid
Inhibits the active reabsorption of
uric acid from renal tubule
Promotes its excretion
Tophaceous deposits are resolved
Relief from arthritis
No analgesic or anti-inflammatory
action
Ues
Chronic gout
With plenty of water & urinary
alkalinizer
Secondary hyperuricaemia
Allopurinol is preferred
Along with penicillin & cephalosporin
Adverse effects
GIT upset
Allergic dermatitis
Sulfinpyrazone
In subtherapeutic dose inhibits the
excretion of uric acid
In therapeutic dose inhibits the
reabsoption of uric acid
Chances of allergic reactions
Benzbromarone
Reversible inhibitor of tubular
reabsorption of uric acid
Action antagonized by sulfinpyrazone
Used in patients with allergic or
refractory to probenecid or
sulfinpyrazone
Benzbromarone + allopurinol more
effective than either drug alone
Thank you