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Purines are natural substances found in all of the body's cells, and in virtually all foods.
The reason for their widespread occurrence is simple: purines provide part of the chemical structure of our genes and the genes of plants and animals When cells die and get recycled, the purines in  their genetic material also get broken down.
Uric acid is the chemical formed when purines have been broken down completely.

Hyperuricemia
The condition when there are high
concentrations of uric acid in the blood.
Serum levels of uric acid are >7mg/dL
(Normally, 2.4-6mg/dL in females; 3.4-
7mg/dL in males)
At such a high level, uric acid tends to
aggregate and form crystals
Primary Hyperuricemia: an innate
defect in purine metabolism and/or uric
acid excretion
Secondary Hyperuricemia: high uric
acid levels due to medications/medical
conditions such as diabetic ketoacidosis,
psoriasis, chronic lead poisoning


Most uric acid dissolves in blood and travels to the kidneys, where it passes out in urine.
If your body produces too much uric acid
or doesn't remove enough if it, you can get
sick.
High levels of uric acid in the body is
called Hyperuricemia.

Uric Acid
Uric acid is the end product in purine metabolism
Excretion of uric acid removes nitrogenous wastes from
body
2/3 of uric acid made is excreted via kidneys; 1/3 via Gl
tract
Urate: protonated form of uric acid


> Uric acid can accumulate due to:
> Overproduction of purine nucleotides
^ Enhanced cell turnover (purine degradation)
^ Decreased in purine salvage pathway
> Underexcretion of uric acid
> Predisposition to many diseases
> People may live with elevated uric acid levels
without experiencing any symptoms

GOUT
Gout and gouty arthritis
• Transient attacks of acute arthritis initiated by
crystallization of urates and neutrophils, followed
by chronic gouty arthritis with tophi in joints and
urate nephropathy
• Sites: 50% have initial attack in first
metatarsophalangeal joint; also ankles, heels,
knees, wrists, fingers, elbows

Gout
> Affects less than 0.5% of the population.
> It is a common condition, presenting h. 1-4%
of adult men.
> Due to familial disposition, incidence may be
as high as 80% in families affected by
disorder.


Alcohol and Gout
Oalcohol metabolism contributes to urate retention
Osome red wines contain purines or oxypurines,
which lead to an increased purine load
Oalcohol may contribute to obesity which is
associated with under excretion of uric acid
O Patients with a history of gout are advised to
drink plenty of fluid, approximately 2 litres per
day (nonalcoholic).


GOUT
• Primary gout (90%): idiopathic with
overproduction of uric acid
• Hyperuricemia in the absence of other
disease
OAsymptomatic hyperuricemia can precede gout
• Impaired secretion by kidneys

• Secondary gout (10%): increased nucleic acid
turnover due to
• chronic renal disease,
• HGPRT deficiency^ hypoxanthine-guanine
phosphoribosyl transferase deficiency)
• Tumors
O Leukemias
O Lymphomas
O After chemotherapy
• Alcoholism
O Accelerated ATP catabolism

GOUT
• Arthritis: synovial fluid is poorer solvent for sodium
urate than plasma, so with hyperuricemia.
• Urates in joint fluid crystallize, particularly in ankle due
to lower temperature; crystals develop in synovial lining
cells, stimulate formation of antibodies, which
accelerates formation of new crystals.
• Release of crystals attracts neutrophils and complement,
(generates c3a, c5a, attracts more neutrophils),
• Releases free radicals, releases lysosomal enzymes

GOUT
^ This will eventually causes acute arthritis that last days
to weeks without treatment; repeated attacks of acute
arthritis cause
^ Renal failure, urate stones


Risk factors for gout with Hyperuricemia are:
Age > 30 years,
Male, familial history of gout,
Alcohol use,
Obesity,
Thiazide administration(reduce the clearance of uric
acid)

Pathogenesis
Enzymatic deficiencies and increased
nucleic acid turnover account for only 10%
of gout patients.
Remaining 90% are "primary gout" due to
an unknown defect limiting the ability to
excrete uric acid.

Uric acid normally dissolves in plasma
Poorly soluble in synovial fluid and
precipitates out as MSU crystals
(monosodium urate crystals )