A brief discussion about gout its defination, presentations, etiology, pathogenesis, pharmacotherapy.

1. GOUT
(GOUTY ARTHRITIS)
FOUZIYA BEGUM
PHARM D

2. DEFINITION:
 The term gout describes a heterogeneous clinical spectrum of diseases
including elevated serum urate concentration (hyperuricemia usually more
than 7.0 mg/dL (416 μmol/L) for men and 6.0 mg/dL (357 μmol/L) for
women), recurrent attacks of acute arthritis associated with monosodium
urate crystals in synovial fluid leukocytes, deposits of monosodium urate
crystals (tophi) in tissues in and around joints, interstitial renal disease,
and uric acid nephrolithiasis(kidney stones)
 Gout is a type of inflammatory arthritis characterised by severe pain,
redness and tenderness in joints.

3. EPIDEMIOLOGY
 Epidemiologic data indicate that the prevalence of gout is also increasing in
less industrialized Eastern countries.
 5 – 7 Numerous factors may explain this finding, including increased
longevity, dietary habits, and increasing prevalence of obesity and the
metabolic syndrome.
 The incidence of gout is consistently higher for individuals who are obese
or who consume large amounts of alcohol or higher amounts of meat or
fish.
Risk factors :
 Elevated serum urate levels are the single most important risk factor for the
development of gout

4. ETIOPATHOGENESIS :
 Several conditions are associated with either decreased renal clearance or an
overproduction of uric acid, leading to hyperuricemia.

5. Overproduction and underexcretion of uric acid :
Over production :
The purine metabolism (fig 102-1) leads to production of either nucleic acid or uric acid. Dietary
purines play an unimportant role in the generation of hyperuricemia in the absence of some
derangement in purine metabolism or elimination.
Two enzyme abnormalities resulting in an overproduction of uric acid have been well described (
Fig. 102–1) .
The first is an increase in the activity of phosphoribosyl pyrophosphate (PRPP) synthetase, which
leads to an increased concentration of PRPP. PRPP is a key determinant of purine synthesis and uric
acid production.
The second is a deficiency of hypoxanthine-guanine phosphoribosyltransferase (HGPRT). HGPRT
is responsible for the conversion of guanine to guanylic acid and hypoxanthine to inosinic acid.
These two conversions require PRPP as the cosubstrate and are important reactions involved in the
synthesis of nucleic acids.
A deficiency in the HGPRT enzyme leads to increased metabolism of guanine and hypoxanthine to
uric acid and to more PRPP to interact with glutamine in the first step of the purine pathway.

6. Underexcretion :
normally, uric acid does not accumulate as long as production is balanced with
elimination. The vast majority of patients (80% to 90%) with gout have a relative
decrease in the renal excretion of uric acid for an unknown reason (primary
idiopathic hyperuricemia).
This are some drugs table (102-2)which decreases the renal clearance of uric acid
through modification of filtered load or one of the tubular transport processes(

8. PRESENTATION OF ACUTE GOUTY ARTHRITIS:
General:
 Gout classically presents as an acute inflammatory
monoarthritis.
 The first metatarsophalangeal joint is often involved
(“podagra”), but any joint of the lower extremity can be
affected and occasionally gout will present as a
monoarthritis of the wrist or finger.
 The spectrum of gout also includes nephrolithiasis(kidney
stones), gouty nephropathy, and aggregated deposits of
sodium urate (tophi) in cartilage, tendons, synovial
membranes, and elsewhere.
 Signs and Symptoms
Fever, intense pain, erythema, warmth, swelling, and
inflammation of involved joints

10. DIAGNOSIS:
 Laboratory Tests : Elevated serum uric acid levels; leucocytosis
 Other Diagnostic Tests :Observation of monosodium urate(MSU) crystals in
synovial fluid or a tophus
 For patients with long-standing gout, radiographs may show asymmetric
swelling within a joint on or subcortical cysts without erosions
MSU crystals in polymorphonuclear
leucocytes in synovial fluid.

11. GOAL OF THERAPY
 The goals in the treatment of gout are to terminate the acute
attack, prevent recurrent attacks of gouty arthritis,
 prevent complications associated with chronic deposition of
urate crystals in tissues, and
 prevent or reverse features commonly associated with the
illness including obesity, elevated triglycerides, and
hypertension.

12. NON PHARMACOLOGICAL TREATMENT:
 to reduce their dietary intake of saturated fats and meats high in purines (e.g., organ
meats)
 Because of the increased risk of developing nephrolithiasis, clinicians should
counsel patients with gout to increase fluid intake and decrease salt consumption
 In addition, joint rest for 1 to 2 days should be encouraged, and local application
of ice may be beneficial.
 Weight loss through caloric restriction and exercise
 Restriction of alcohol intake
 Joint exercise and application of heat to the affected area should be avoided, as
they can worsen the condition.
 NOTE:The presence of gout should not be a contraindication to the use of thiazide
diuretics in hypertensive patients

13. PHARMACOTHERAPY:

16. Reference:Pharmacotherapy A Pathophysiologic Approach
Eighth Edition by joseph dipiro
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