Metabolic disorder affecting jts & soft tissues.
- Assocd w hyperuricemia.
- Hyperuricemia is either primary [familial or sporadic] or secondary to an acquired condition, genetic disorder or drug treatment.
- ~ 10% of individs w hyperuricemia --> gout.
Primary hyperuricemia accounts for ~90% of all cases of gout and ~90% of these are due to reduced renal excretion of urate.
Hyperuricaemia may also be secondary to disorders that increase the production of uric acid by cell breakdown, myeloproliferative disorders or disorders that decrease the secretion of uric acid (chronic renal failure).
Gout char'd by episodic acute attacks of inflam, usu monoarticular arthritis, and chronic deposition of deposits of sodium urate around affected joints.
Uric acid = end product of purine catab, (component of nucleic acids. Increased synth of uric acid / dc secretion of uric acid by the kidneys --> hyperuricaemia.
Uric acid not v soluble --> ppts above certain conc's. Prolonged hyperuricaemia --> deposition of urate crystals in joints and tissues.
Crystals--> provoke acute inflam rxn.
- Gout divided into various clin stages:
- - Acute gouty arthritis,
- - Chronic stage in which diffuse deposits are seen i.e. chronic tophaceous gout.
The acute arthritis is char'd by swollen painful joint (often the big toe), rapid clinical onset, low grade fever and leucocytosis.
- Microscopic examination of synovial fluid reveals inflam exudate and presence of -vely birefringent needle shaped crystals and polymorphs.
- The chronic chalky tophi are deposited around joint.
The crystalline deposits are ringed by characteristic collections of histiocytes and multinucleate giant cells
Examination under polarised light ---> needle shaped crystals...typical birefringence pattern of monosodium urate. Alcohol preservation allows visualisation of crystals.
- chronic urate nephropathy
- uric acid calculi.