Gout and Hyperuricemia Flashcards
gout
inflammatory arthritis that develops in people who have increased uric acid in the blood
uric acid forms needle like cyrstals in joints and cause sudden and severe episodes of pain
clinical progression of gout
1 asymptomatic hyperuricemia
- acute gouty arthritis
- interval/intercritical gout
- chronic trophaceous gout
asymptomatic hyperuricemia
no dug therapy just monitor
Only 20% of pts with elevated uric acid develop gout
acute gouty arthritis
inflammatory response, treatment needed
b. Must be differentiated from:
i. Pseudogout – build up of calcium deposits
ii. Acute septic arthritis – joint aspiration
NSAID(indomethacin, naproxen, sulindac)
colchicine,
corticosteriods
interval/intercritical gout
time period in between attacks
Prophylactic or anthyperuricemic therapy
colchicine
chronic trophaceous gout
long term buildup of uric acid:
Solid urate in connective tissue
Very rare due to effective meds
If untreated 60% of pts will develop tophi
Risk factors: poor compliance with medication, chronic renal insufficiency
risk factors for acute gouty arthritis
trauma/surgery,
alcohol consumption,
dietary overindulgence,
drugs (diuretics, low dose ASA, Niacin, cyclosporin),
rapid lowering of uric acid (allopurinol)
GOAL of treatment
relieve pain and inflammation
do not start or stop hypouricemia drugs until 3 weeks after acute attack: immobilzation of uric acid and drugs will mobilize it
it will increase uric acid in blood = increase risk of acute attack
prophylactic therapy
severe attacks of gouty arthritis
complicated course of uric acid nephrolithasis
substantially increased serum uric acid (>10mg/dl)
24 hr urinary excretion of uric acid more than 1000mg
do not initiate anti-hyperuricemic agents unless:
pt has frequent acute attacks (1-2/yr)
clinical radiographic signs of acute gouty arthritis
presence of tophacous deposits
evidence of urate nephroliathasis
Tx options
NSAIDS
colchicine
corticosteriods
NSAIDS
indomethacin, naproxen, sulindac
MOA: inhibitng COX-2 metiated PGs and syntheisis at site of injury
USE: acute gout attack
dangerous in prophlyaxis
Cholchicline
reduced inflammatory response to depsoited crystals
diminished PMN phagocytosis of crystals
blocks cellular response to depsotied crystals
CYP450 3A4 involved in metabolism
USE: acute gout attack, prophylaxis
ADR: GI intolerance, heme/penias, hepatomeagly (inc LFT), myopathy
drug interactions: Strong 3A4 inhibitors, p-pg inhibitors,s tatins, fibrates, dogoxin
corticosteriods
prednisone
acute gouty attack when reistsent to toher therapy ot pt cannot tolerate NSAIDs
antihyperuricemic drugs
uricosuric agents (probenecaid)
xanthine oxidase inhibitors (allopurinol, febuxostat)
uric acid trabnsporter inhibitors (lesinurad, pegloticase, rasburicase)
uricosuric agents
probenecaid
USE: normal renal function, under excrete uric acid, negative hx of nephrolithias
MOA : antagonist of URAT1 transporter to block uric acid reabsorption -> increase uric acid secretion
ADR: precipiation of acute attack, nephroliathisis, GI intolerance, hypersenstivity reactions
NOT EFFECTIVE in over producers
Xanthinine oxidase inhibitors
allopurinol (high risk first line) , febuxostat (intol to allo)
MOA: inhibits breakdown of xanthinine into uric acid
effective for over and under excreters
ADR: hypersensitivity reactions, allopurinol desensitization
drug interactions: azathiopurine mercaptopurine ACEI Warfarin
uric acid transport inhibitor
lesinurad
pegloticase, rasburicase
lesinurad
uric acid transport inhibitor
MOA: inhibit URAT1
used in combo with xanthinine oxidase inhibitors for hx of hyperuricemia
ADR: not monotherapy
petloticase
indicated for adult pts who are refractory to conventional therapy
MOA: catalyzes oxidation of uric acid to readily eliminated metabolite
ADR: anaphylaxis, infusion reactions, G6PD deficency assoc with hemolysis, methmeglobinemia
rasburicase
hyperuricemia due to malignancy in pts with risk of tumor lysis syndrome
MOA: catalyzes oxidation of uric acid to readily eliminated metabolite
ADR: anaphylaxis, infusion reactions, G6PD deficency assoc with hemolysis, methmeglobinemia