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Copy of Hyperuricemia (Gout)

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Sujood AbuDaia

on 9 May 2016

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Transcript of Copy of Hyperuricemia (Gout)

What is Gout?
Gout is a kind of arthritis caused by a build-up of uric acid crystals in the joints. Uric acid is a breakdown product of purines that are part of many foods we eat.
The root cause of gout is hyperuricemia and it is characterized by recurrent attacks of acute inflammatory arthritis. The formation of urate crystals leads to the formation of tophaceous deposits (sandy, gritty, nodular masses of urate crystals), particularly in the joints which precipitates the episodes of gouty arthritis.
Gouty arthritis is the most painful manifestation of gout and is caused when urate crystals interact with neutrophils triggering an inflammatory response
Risk factors of Gout
Obesity, excessive weight gain, especially in youth, moderate to heavy alcohol intake, high blood pressure, and abnormal kidney function are among the risk factors for developing gout.
Certain drugs and diseases can also cause elevated levels of uric acid. Also, there is an increased prevalence of abnormally low thyroid hormone levels (hypothyroidism) in patients with gout.

Hyperuricemia (Gout) is defined when the serum uric concentration is more than 6 mg/dl in female or more than 7 mg/dl in male, where the normal serum uric concentration is:
2-6 mg/dl in female.
3-7 mg/dl in male.

So, in order to understand how does gout develop, let's know how purine nucleotides occur which is the main source of uric acid
Purine Catabolism
1. Primary gout: due to a disorder of purine metabolism
2. Secondary gout: is due to a complication or as a result of another condition that caused the development of the disease.
Symptoms of gout
Acute gout attacks are characterized by a rapid onset of pain in the affected joint followed by warmth, swelling, reddish discoloration, and marked tenderness.
The small joint at the base of the big toe is the most common site for an attack. Other joints that can be affected include the ankles, knees, wrists, fingers, and elbows.
These painful attacks usually subside in hours to days, with or without medication. In rare instances, an attack can last for weeks. Most people with gout will experience repeated bouts over the years.
Kidney stones are more frequent in people with gout.
Hyperuricemia (Gout)
it may as a result of :
1. HGPRT Deficiency "Lesh Nyhan Syndrom"
due to deficiency in Hypoxanthine, Guanine-phosphoraibosyl Transferase enzyme
2. Renal disease: due to decrease excretion of uric acid in urine
causes of gout
secondary gout
Primary Gout
it is a disorder of purine metabolism leads to over production of purine due to mutation of PRPP-Synthetase enzyme.
a mutant enzyme without its allosteric site the enzyme is non sensitive to the (-ve) feedback inhibition by AMP, GMP & IMP purine de novo synthesis
4.Cancer & leukemia: due to increase tissue turnover increase degradation of DNA increase uric acid
3. Excess alcohol intake: that means more lactic acid in urine insted of uric acid
5. Glucose 6-phosphate Deficiency " Von Gierkes Disease":
increase glucose 6-P in liver increase Ribose 5-P
increase PRPP increase purine synthesis increase uric acid.
6. Excess intake of food rich in proteins.
Lesch-Nyhan syndrome
is inherited as an X-linked recessive of Hypoxanthine Guanine Phosphoribosyl Transferase (HGPT),
it's more common in male than in female.

It is characterized by:
1. hyperuricaemia
2.mental retardation and neurological symptom : due to decrease DNA synthesis
3. self-mutilation: Lip/Finger Biting
Hyperuricaemia is due to decreased activity of the salvage pathway causing decreased purine reutilization and increased uric acid synthesis. Relatively low levels of nucleotides result in decreased inhibition of de novo synthesis, resulting in further overload of the non-functioning salvage pathway and increased uric acid production.

2. Probenecid: increase uric acid excretion in urine " uricosuric agent"
3. Correction of feeding habit :
they can used to prevent acute attack of arthritis because colchicine inhibits phagocytosis of uric acid crystals by polymorphs inhibition of release of chemotactic substances inhibit occurenc of inflammation
1. Allopurinol
Treatment of gout
Treatment for gout usually involves medications .
Gout medications can be used to treat acute attacks and prevent future attacks as well as reduce your risk of complications from gout, such as the development of tophi from urate crystal deposits.

it causes competitive inhibition of xanthine oxidase enzyme because allopurinol is hypoxanthine analog.
Irreversible inhibition "Suicide inhibition"
* food rich in nucleotide and nucleic acid e.g liver &meat are avoided in diet.
*Relative reduction of the amount of protein in diet.
1. Allopurinol "Irreversible inhibitor"
4. Colchicine & non steroidal anti-inflammatory drugs : e.g. Aspirin & Endomethacin.
5. Alkalinization of urine to solubility of uric acid in urine.
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