Download MBBS Gout Lecture PPT

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