4. Gout MT1 Flashcards
this is an inflammatory disease associated with the deposition of monosodium urate crystals (MSU) in joints and soft tissues due to chronic hyperuricemia
gout
this is when the serum is saturated with monosodium urate. concentrations are above/around 416 micromols/L for men and 357 micromols/L for women
hyperuricemia
true/false: sustained elevation of serum urate is essential for the development of gout, but hyperuricemia does not always lead to gout
true
what are some risk factors for developing gout?
- male gender
- increased age
- obesity, sedentary lifestyle
- consumption of alcohol, surgery beverages, and red meat (food high in purines)
_______ is the final step in the degradation of purines. this has no physiological purpose, and it is a waste product.
uric acid
our body makes these endogenously and we can also get them exogenously from food; makes up building blocks of DNA and RNA.
purines
hyperuricemia will occur when there is either _______ or ________ of uric acid
overproduction or under excretion
this is the less common cause of hyperuricemia; is occurs when there is an issue with the enzyme systems that regulate purine metabolism (increase in PRPP synthase which is a key determinant of purine synthesis in the body and a decrease in HGPRT); usually seen in blood cancers where there is an excessive rate of cell turnover
overproduction of uric acid
this is a more common cause of hyperuricemia and gout; 90% of gout patients have a relative decrease in the renal excretion of uric acid for an unknown reason; sodium reapsorbtion may also be linked to this (dehydration - body saves Na which in turn saves uric acid and therefore not as much is excreted); drug can also hinder excretion
under excretion of uric acid
what are some common drugs than can modify filtration or uric acid or alter reabsorption
- alcohol
- cyclosporines
- diuretics: thiazide (HCTZ, chlorthalidone and indapamide) and loop (furosemide)
- tacrolimus
what are the 4 different clinical spectrums of gout?
- asymptomatic hyperuricemia
- acute gouty arthritis (gouty flare)
- intercritical gout (prophylaxis of flares)
- chronic gouty arthritis
this is not an indication for uric acid lowering therapy
- try to identify possible cause and eliminate medications that could be contributing
- encourage lifestyle modifications
asymptomatic hyperuricemia
this is a rapid localized onset of excruciating pain, swelling and inflammation. the attack is usually monoarticular - most often in the metatarsophalangeal joint (big toe)
insteps > ankles>heels>knees>wrists>fingers>elbows
fever and elevated WBCs may be seen
acute gouty arthritis (gouty flare)
does this describe a presumptive or definitive diagnosis?
for typical presentation clinical diagnosis is alone reasonable (elevated serum uric acid + inflammation/pain of the big toe)
presumptive diagnosis
does this describe a presumptive or definitive diagnosis?
presence of crystals in the synovial fluid
definitive diagnosis
treatment for an acute episode of gout should be treated within ____ hours of symptom onset
24
what are the three options for treating an acute episode of gout?
- nsaids
- colchicine
- corticosteroids
ture/false: treatment options (e.g. NSAIDS, colchicine and corticosteroids) can be combined in order to treat an acute episode of gout in those with severe gout
true BUT avoid the use of an oral steroid + NSAID due to increased risk of GI adverse effects
true/false: you should not use NSAIDs concomitantly, even with low dose aspirin
false - can use with appropriately indicated low dose ASA
what are the most commonly used NSAIDs for gout?
indomethacin
naproxen
ibuprofen
celecoxib
if a patient is taking an NSAID for an acute gout flare, how long after starting the NSAID should they wait to see a HCP if the pain doesn’t get better
5-8 days
this medication is only effective if its started within 36 hours of symptoms, with the greatest efficacy seen in the first 24 hours of symptom onset
colchicine