gout
crystal deposits of uric acid in joints –> damage to joints d/t inflm
uric acid
nitrogenous waste product usually processed in liver & excreted by kidney
primary form (90%)
secondary form
why does accum of uric acid occur in secondary form
d/t kidneys not excreting uric acid & continuing to retain it
example of “condition” that leads to excessive cell turnover (secondary form)
chemotherapy (Tx for CA) –> uric acid is byproduct of cell breakdown
why does alcohol abuse cause secondary form
Purines & pyrimidines are nitrogenous bases joined by hydrogen bonds (A, C, G, T in DNA & U instead of T in RNA)
patho
stages
1) hyperuricemia (asympt)
2) acute inflm in 1 joint (big toe)
3) acute inflm subsides in approx 1 wk
4) pt asympt for mo-yrs
5) frequent recurrent attacks –> permanent damage
stage 2 in gout precipitating events
stage 2 in gout characteristics
Dx
- X-ray
Tx for acute attacks
Tx for long-term attacks
colchicine
anti-mitotic properties not utilized, drug used for anti-inflm properties and inhibits migration of leukocytes into joints (WBCs engulf uric acid, gets lysed, and reases harmful Es… colchicine blocks this action)