Introduction, Pathogenesis, signs and symptoms, treatment and diagnosis test

1. Dreamz College of Pharmacy
Gout
Mrinal
Assistant Professor
Pharmacology

2. Introduction
• Gout is a common arthritis caused by deposition of monosodium urate
crystals within joints after chronic hyperuricaemia
• It affects 1–2% of adults in developed countries& is the most common
inflammatory arthritis in men.
• Epidemiological data are consistent with a rise in prevalence of gout.
• Diet / genetic polymorphisms of renal transporters of urate seem to be
the main causal factors of primary gout.
• Gout & hyperuricaemia are associated with HT, DM, metabolic syndrome,
renal & CVD.
• Interleukin β is a pivotal mediator of acute gout & could become a
therapeutic target.
• When serum uric acid is lowered below monosodium urate saturation
point (2.4-6.0 mg/dL) female and 3.4-7.0 mg/dL) male, the crystals
dissolve & gout can be cured.

3. Introduction
• Uric acid loses its proton, then binds sodium and convert into monosodium
urate crystals at pH 7.4
• Uric acid is poorly soluble in body fluids and excrete out in blood and urine
• Hyperuricemia when level of uric acid exceed its solubility in body fluids.
• Hyperuricaemia and gout may be classified into 2 types: metabolic and
renal, each of which may be primary or secondary.
• Primary refers to cases in which the underlying biochemical defect causing
hyperuricaemia is not known, while secondary denotes cases with known
cause.
1. Hyperuricaemia of metabolic origin. This group comprises about 10%
cases of gout which are characterised by overproduction of uric acid.ses
of hyperuricaemia.
2. Hyperuricaemia of renal origin. About 90% cases of gout are the result of
reduced renal excretion of uric acid. Altered renal excretion could be due
to reduced glomerular filtration of uric acid, enhanced tubular
reabsorption or decreased secretion.

4. Introduction
• Acute gout
Painful arthritic attack of sudden onset.
Usually occurring at night or in early morning
Arthritic pain worsen progressively
Generally involves one or few joints
Most common site of initial attack metatarsophalangeal joint.
Other sites ankle, heel, knee, wrist, elbow and fingers.
• Chronic Gout
Frequency of attacks increases, continuous deposit leads to damage joints
and chronic pain
Patients may develop large subacutenous tophi (Stones) in pinna of
external ear, eyelids, nose and around joints (image on next ppt)
The ureate crystals in kidney leads renal disease.
Articular cartilage may be destroyed result in joint deformities

5. Tophi

6. Etiology
• Increased cosumption puriens
Sea food, red meat, organ meat
• Increased production of puries
High fructose corn syrup beverages
• Decrease clearence of uric acid
Dehydration (not enough water/ alcohol consumption)
• Obesity and diabetes
• Chemotherapy and radiation (leads to cell death nucleic acid degradation)
• Genetic predisposition
• Chronic kidney disease
• Medications (Thiazides diuretics, asiprin)

7. Signs and Symptoms
• First metatarsal Joint of big toe
Podagra – Wakes up feeling like toe on fire
Pain most severe in hours after attack lessen with time
Can last for days and weeks
• Affect other joints as well
Knee, ankle, wrist, elbow
Basicall the inflammation caused by white blood cells

8. Uric acid synthesis and excretion

10. How we diagnose Gout

11. Other diagnostic tests
• Serum Uric level analysis
• 24 Urine collection for uric acid
determination
urinary levels are normal below 750mg/24h
Above this level means gout

12. Treatment
• Decrease pein and swelling
NSAID (ibuprofen and naproxen sodium)
Corticosteroids
Colchicine (inhibits WBC migration)
• Treating underlying cause
Diet modification
• Decrease uric acid levels
Xanthine oxidase inhibitors (allopurinol)
Uricosuric medication (Probenecid - Increase
excretion of uric acid by kidney)