gout home remedies

Gout is a disorder that manifests as a spectrum of clinical and pathologic features built on a
foundation of an excess body burden of uric acid, manifested in part by hyperuricemia, which is
variably defined as a serum urate level greater than 360umol/l (6.8mg%)

The term gout is derived from the latin word 'guta' meaning a drop, and originally may have referred to a drop of poison or evil humor.
? a group of diseases characterized by hyperuricaemia and uric acid crystal formation.

Gout is a disease in which tissue deposition of monosodium urate (MSU) crystals occurs due to hyperuricemia (MSU supersaturation of extracellular fluids) Occur at >360umol/l concentration

These clinical syndromes include Asymptomatic hvperuricaemia
Acute ooutv arthritis,
tophaceous pout,
uric acid nephrolithiasis, and
outv nephrooath
:*ln its more narrow and perhaps more commonly
used definition, gout refers to arthritis caused by
uric acid crystals.


CHARACTERISTICS OF AN ACUTE
ATTACK OF GOUT
• Early episodes of acute gouty arthritis are typically monoarticular (85%) and begin abruptly, often during the night or early morning.
• The affected joint becomes exquisitely painful, warm, red, and swollen.
• A low -grade fever may be present.
• The periarticular erythema and swelling may progress to resemble a cellulitis termed gouty
cellulitis.


Pathophysiology
uric acid is an end product of purine biosynthesis.
Hyperuricaemia is a necessary but not a
sufficient condition for the development of
gout;
and although the mechanisms of excess uric
acid accumulation are well defined, the
subsequent phases of crystal formation and
release into tissues remain less well
characterized.


purine metabolism
Purines are derived from two sources.
(1) ingested in food
(2) generated via a complex de novo synthetic pathway.
Components of the purine ring are complexed to the
donor     substrate phosphoribosylpyrophosphate (
PRPP).
These are then taken through a 10-step process
culminating in purine nucleotide formation.
PRPP is also used as a substrate for pyrimidine and
pyridine synthesis. Thus, the first committed step in
purine synthesis is catalysed by the enzyme
amidophosphoribosyl transferase (amidoPRT).

ric acid metabolism
¦ Uric acid is ultimately formed from purine nucleotides
through the intermediate compounds xanthine,
hypoxanthine, and guanine by the enzyme xanthine
oxidase.
¦ It is a terminal product as no mammalian uricase
exists.
Uric acid is made primarily in the liver.
The average pool size is 1200 mg in men and 600 mg in
women.
In both men and women, about two-thirds of the total uric


Causes of secondary gout
cid, such as tumour
lysis syndrome, myeloproliferative disease,
haemolytic amaemia, and psoriasis.
All of these conditions are characterized by
increased cell turnover with a subsequent increase
in purine synthesis and catabolism.
*) Undersecretion of uric acid
> such as renal failure and many drugs
> Lead exposure is a cause of secondary gout.
Saternine gout, which is associated with heavy lead
exposures (often from the ingestion of lead-laden
whisky), is rare today.