Download MBBS Gout Lecture PPT

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hyperuricemia that results the formation of uric

acid crystals depositing in especially joints and

tissues of the body which causes inflammation.

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? HYPERURICEMIA --
?
? over production,
? under secretion or

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combination of two.
GOUT.

? Gout is a metabolic disorder characterized by

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hyperuricemia due to defective purine metabolism.

? Hyperuricemia can lead to deposition of sodium urate

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crystals especially in joints and kidney.

? Types-
? Acute--
? it manifest as sudden onset severe

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inflammation in a small precipitation of urate crystals

in joint spaces.

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? Chronic --
? when pain and stiffness patient persist in a joint

between attack, gout becomes chronic.
ETIOLOGY.

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? Gout occurs due to defective metabolism in

which uric acid is the end product.

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? Main cause of hyperurecemia-
? Overproduction of uric acid
? Excessive turn over of nucleoproteins.
? Excessive dietry purines
? Excessive synthesis of uric acid to rare enzyme

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defect enzyme mutation defect.

? Under excretion of uric acid
? Defect in renal excretion

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? Inborn errors of metabolism.
Predisposing factor.

? Purine rich foods.
? Caffeine.

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? Drugs.
? Alcohol.
? Trauma.
? Disease
? a. Lesch ? Nyhan sundrome

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? b. Von-Gierke's disease.
? c. Syndrome X
? Genetic disease.

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ACUTEGOUT.
CHRONIC GOUT.

? Site of tophi include:
? 1st MTPJ (PODOGRA).

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? Digits of the hand and feet ( most common).
? Bursa around elbows and knees.
? Achilles tendon
? Pinna of the ear.
CHRONIC GOUT.

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? SIGN AND SYMPTOMS-
? Joint damage
? Joint pain
? Joint stiffness

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? Articular cartilage may be destroyed resulting

in joint deformites.

? Patient may develop large subcutaneous

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Tophi.
GOUT.

? Group of disorder presented with

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? 1.Hyperuricemia
? 2.uric acid nephrolithesis.
? 3. Acute inflammatory Arthritis.
? TWO TYPES--
? 1.primary gout--

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? due to defect in the enzymess that lead

to over production of purine nucleotides.

? Super activity PRPP synthetase.

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? Deficiency HGPRTase( Lesh-Nyhan syndrome).
? G6PD(Type-1 glycogen storage disorder).
GOUT.

? 2. Secondary gout--

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? A. Increased production of

uric acid

? Leukemia

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? Lymphoma
? B.Decreased excretion
? Renal failure
? Thiazides
? diuretics

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PURINE DEGRADATION.
Clinical presentation

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? STAGES
? Stage-1 : Asymptomatic hyperuricemia
? Stage-2 : Acute gout attack
? Stage-3 : Intercritical period
? Stage-4 : chronic tophiceous gout.

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CLINICAL PRESENTATION.

? Symptomps-
? Severe pain, swelling and warmth in the affected joints.
? The attack is usually monoarticular and the most

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common sites are metatarsophalangeal joints of big

toe.(Acute gouty Arthritis).

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? Signs-
? Affected joints are warm, red and swellen.
? Mild fever may present.
? Tophi ( mono-sodium urate crystals) may present in

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chronic cases.
Laboratory.

? Hyperuricemia
? Biochemical hallmark of gout, but not by itself

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diagnostic for gout.

? Leukocytosis.
? Increased ESR.

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? Synovial Fluid-
? MSU needle
? ? like intracellular and extracellular crystals.
? Negatively birefringent needle shaped monosodium

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urate crystals under polarised light microscopy.


INVESTIGATION.
INVESTIGATION.

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? to detect the presence of medical condition

associated with gout/ hyperuricemia ?

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? Full blood count/differential count--

? To exclude infection or myeloproliferative disease.
? Serum creatinine/ urea--

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? To exclude hyperuricemia due to renal diseaese.
? Serum uric acid-hyperurecemia is not equivalent to gout.
? Blood glucose--- to exclude DM.
? Lipid profile
? Urinanalysis.

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INVESTIGATION

? Specific investigation for confirmation of of

gouty arthritis.

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? Joint aspiration and crystal identification.
? Serum urate.
? To detect complication
? Renal imaging

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? Skeletal x ? rays.
Synovial fluid Examination.
COMPLICATION OF GOUT.
TREATMENT GOUT.

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ACUTE

CHRONIC

GOUT.

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GOUT

NSAID

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URICOSURIC

COLHICINE

PROBENECID

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SULFINPYRAZONE

SYNTHESIS INHIBITOR

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ALLOPURINOL (XANTHINE OXIDASE

CORTICOSTEROID

INHIBITOR).

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FEBUXOSTAT.