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Gout Presentation Group 2
Gout Presentation Group 2
Valentine Mhute
Kingston Gwekwe
Tadiwa Chidavaenzi
Tadiwa Maimba
Linda Chipango
Moyo Vitalis
Harder Dorcas
Definition
• Gout refers to a metabolic disorder characterized
by increased deposition of urate crystals in the
joints and connective tissue (tophi) and results in
episodic acute or chronic arthritis.
• Is also a common form of inflammatory arthritis
that is very painful. It usually affects one joint at a
time (often the big toe joint).
• There are times when symptoms get worse, known
as flares, and times when there are no symptoms,
known as remission.
• It also leads to deposition of urate crystals within
the renal interstitium or nephrolithiasis.
• Signs and Symptoms • Risk Factors
• Swelling in joints, • Being male (more common in men than women)
• Overweight
• Pain, usually intense
• Family history
• Redness • Medications, e.g. diuretics
• Fever • Excessive consumption of alcoholic beverages such
as beer.
• Poor mobility
• Eating or drinking food and drinks high in fructose
• Tenderness • Diet: Having a diet high in purines, which are
• Flulike symptoms metabolised into uric acid. Purine-rich foods include
red meat, organ meat, and some kinds of seafood,
• Tenderness such as shellfish and tuna.
• Health conditions including: diabetes mellitus,
congestive heart failure (CHF), renal insufficiency
(poor kidney function)
Metabolic pathway of Uric Acid production
Metabolic pathways of uric acid formation from nucleotide monophosphates. AMP, adenosine monophosphate; IMP,
inosine monophosphate; XMP, xanthine monophosphate, GMP, guanine monophosphate.
Pathophysiology
• Uric acid is end product of purine metabolism and is
excreted by the kidneys
• Hyperuricemia results from:
-Increase in uric acid production
-Underexcretion of uric acid by kidneys
• Both: diet high in purines will not cause gout, but may trigger
an attack in a susceptible person
Management of Gout
• Acute Gout • Chronic Gout
-Colchicine • Collaborative Care Prevention of acute
-NSAIDS (Indomethacin, attacks:
Diclofenac, Naproxen, Etoricoxib) • Urate Lowering Drugs
• Allopurinol
• Corticosteroids (Prednisolone)
• Febuxostat
• Probenecid
• Sulfinpyrazone
Management Continued
• Colchicine
MOA: Reduce lactic acid production by leukocytes, which in turn decreases uric acid deposition and reduces
phagocytosis, with abatement of the inflammatory response.
• Uses: Terminating acute attack, 0.6-1.2mg, then 0.6mg every 2-3hrs.
• Adverse effects: diarrhoea, abdominal pain