Download MBBS (Bachelor of Medicine and Bachelor of Surgery) Latest Gout Lecture PPT
What is Gout.
? Gout is painful condition associated with
hyperuricemia that results the formation of uric
acid crystals depositing in especially joints and
tissues of the body which causes inflammation.
? HYPERURICEMIA --
?
? over production,
? under secretion or
combination of two.
GOUT.
? Gout is a metabolic disorder characterized by
hyperuricemia due to defective purine metabolism.
? Hyperuricemia can lead to deposition of sodium urate
crystals especially in joints and kidney.
? Types-
? Acute--
? it manifest as sudden onset severe
inflammation in a small precipitation of urate crystals
in joint spaces.
? Chronic --
? when pain and stiffness patient persist in a joint
between attack, gout becomes chronic.
ETIOLOGY.
? Gout occurs due to defective metabolism in
which uric acid is the end product.
? Main cause of hyperurecemia-
? Overproduction of uric acid
? Excessive turn over of nucleoproteins.
? Excessive dietry purines
? Excessive synthesis of uric acid to rare enzyme
defect enzyme mutation defect.
? Under excretion of uric acid
? Defect in renal excretion
? Inborn errors of metabolism.
Predisposing factor.
? Purine rich foods.
? Caffeine.
? Drugs.
? Alcohol.
? Trauma.
? Disease
? a. Lesch ? Nyhan sundrome
? b. Von-Gierke's disease.
? c. Syndrome X
? Genetic disease.
ACUTEGOUT.
CHRONIC GOUT.
? Site of tophi include:
? 1st MTPJ (PODOGRA).
? Digits of the hand and feet ( most common).
? Bursa around elbows and knees.
? Achilles tendon
? Pinna of the ear.
CHRONIC GOUT.
? SIGN AND SYMPTOMS-
? Joint damage
? Joint pain
? Joint stiffness
? Articular cartilage may be destroyed resulting
in joint deformites.
? Patient may develop large subcutaneous
Tophi.
GOUT.
? Group of disorder presented with
? 1.Hyperuricemia
? 2.uric acid nephrolithesis.
? 3. Acute inflammatory Arthritis.
? TWO TYPES--
? 1.primary gout--
? due to defect in the enzymess that lead
to over production of purine nucleotides.
? Super activity PRPP synthetase.
? Deficiency HGPRTase( Lesh-Nyhan syndrome).
? G6PD(Type-1 glycogen storage disorder).
GOUT.
? 2. Secondary gout--
? A. Increased production of
uric acid
? Leukemia
? Lymphoma
? B.Decreased excretion
? Renal failure
? Thiazides
? diuretics
PURINE DEGRADATION.
Clinical presentation
? STAGES
? Stage-1 : Asymptomatic hyperuricemia
? Stage-2 : Acute gout attack
? Stage-3 : Intercritical period
? Stage-4 : chronic tophiceous gout.
CLINICAL PRESENTATION.
? Symptomps-
? Severe pain, swelling and warmth in the affected joints.
? The attack is usually monoarticular and the most
common sites are metatarsophalangeal joints of big
toe.(Acute gouty Arthritis).
? Signs-
? Affected joints are warm, red and swellen.
? Mild fever may present.
? Tophi ( mono-sodium urate crystals) may present in
chronic cases.
Laboratory.
? Hyperuricemia
? Biochemical hallmark of gout, but not by itself
diagnostic for gout.
? Leukocytosis.
? Increased ESR.
? Synovial Fluid-
? MSU needle
? ? like intracellular and extracellular crystals.
? Negatively birefringent needle shaped monosodium
urate crystals under polarised light microscopy.
INVESTIGATION.
INVESTIGATION.
? to detect the presence of medical condition
associated with gout/ hyperuricemia ?
? Full blood count/differential count--
? To exclude infection or myeloproliferative disease.
? Serum creatinine/ urea--
? To exclude hyperuricemia due to renal diseaese.
? Serum uric acid-hyperurecemia is not equivalent to gout.
? Blood glucose--- to exclude DM.
? Lipid profile
? Urinanalysis.
INVESTIGATION
? Specific investigation for confirmation of of
gouty arthritis.
? Joint aspiration and crystal identification.
? Serum urate.
? To detect complication
? Renal imaging
? Skeletal x ? rays.
Synovial fluid Examination.
COMPLICATION OF GOUT.
TREATMENT GOUT.
ACUTE
CHRONIC
GOUT.
GOUT
NSAID
URICOSURIC
COLHICINE
PROBENECID
SULFINPYRAZONE
SYNTHESIS INHIBITOR
ALLOPURINOL (XANTHINE OXIDASE
CORTICOSTEROID
INHIBITOR).
FEBUXOSTAT.
This post was last modified on 30 November 2021