GOUT AND PSEUDOGOUT PRESENTATION BY A 5TH YEAR MEDICAL STUDENT. THIS PRESENTATION IS EDUCATIVE. READ AND KINDLY SHARE WITH FRIENDS, LOEVD ONES, MEDICAL PERSONNELS. THANKS.
The acute inflammation of gout is believed to be initiated by the ingestion of uncoated urate crystals by monocytes, leukocytes and synoviocytes.
Once inside the cell, the gout crystals are processed through toll-like receptors and activate NALP-3inflammasomes that in turn release a variety of chemotactic agents and cytokines capable of mediating inflammation.
Majority experience 2nd acute flare within 1 year of first gout flare
Tophus is a nodular deposit of monosodium urate monohydrate crystals with an associated foreign body reaction.
Gout can evolve into a chronic, deforming polyarthritis of upper and lower extremities that mimics rheumatoid arthritis.
The tophi are firm yellow in colour and occasionally discharge a chalky material.
The disease is especially common in Pacific Islanders e.g Filipinos,Samoans.
Primary gout has a heritable component and genome-wide surveys have linked risk of gout to several genes whose products regulate urate handling by the kidney(increased production of purine-Lesch Nyhan syndrome, glycogen storage dx)
Secondary gout, which may have a heritable component is related to acquired causes of hyperuricemia(increased catabolism and turnover of purine) e.g low-dose aspirin, niacin, myeloproliferative disorders, multiple myeloma, lead poisoning, hemoglobinopathies, psoriasis, ALCOHOL.
UCE values will be high
Eating a diet high in low-fat diary products, Vitamin C