Gout Flashcards by Linda Chen

what is gout?

an inflammatory arthritis resulting from deposition of uric acid crystals in tissues and fluids

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what is hyperuricemia

elevated serum urate concentration

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what is acute arthritis

deposition of urate crystals in synovial fluid leukocyets, leading to an inflammatory response

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what are tophi

deposits of monosodium urate crystals in tissues in and around joints

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gout affects
1. more males than females
2. more females than males
3. the population in a bimodale age distribution
4. younger population 10% of the time

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what is the peak age for gout diagnosis

40-50 in males
>60 in females

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is there a genetic link to gout?

yes

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in asymptomatic hyperuricemia, ____ go on to develop acute gout

25%

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what are the 4 steps in the course of gout illness

asymptomatic hyperuricemia
acute gouty arthritis
intercritical gout
advanced gout

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what enzyme is responsible for the production of uric acid

xanthine oxidase

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what is present in animals to break down uric acid, but not in humans

uricase

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causes of primary gout (overproduction)

idiopathic
genetic enzyme abnormalities

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what causes primary gout with underexcretion of UA

idiopathic

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what causes secondary overproduction of UA

excessive dietary intake
increased tissue breakdown (myeloproliferation or lymphoproliferative disorders, hemolytic diseases, psoriasis)

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what causes secondary underexcretion of UA

decreased renal function
metabolic acidosis
dehydration

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list some diet related factors that change SUA

meat, seafood intake
alcohol
high fructose content

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drug related factors that change SUA

increases SUA: salicylates, diuretics, niacin, cyclosporin, tacrolimus, cytotoxic chemo
decreases SUA: allopurinol, febuxostat, probenecid, losartan

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disease related factors that change SUA

CVD, CKD, nephrolithiasis, metabolic sx (obesity, insulin resistance, hyperlipidemia, HPTN)

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what are 3 factors that lower the risk of gout

dairy
coffee (including decaf)
vit C

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acute gouty arthritis is usually ____ and resolves ___________ within ______

usually monoarticular
resolves spontaneously in 7-10d

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what is the clinical presentation of acute gout

rapid onset of pain with warmth, swelling, erythema that escalates over 8-12hrs
usually monoarticular, usually in big toe

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presumptive diagnosis of gout if:

hyperuricemia present
acute monoarticular arthritis
gratifying clinical response to colchicine (complete resolution of sx within 48hrs, no recurrence for at least 1 wk)

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what is intercritical gout

symptom free but urate crystal deposition continues + tophi increase in size

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what is the typical patient of new onset gout

hyperuricemia, postmenopausal women, men >30yrs

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what is the typical patient fo rlong standing fout

elderly men or women

how long do sx usually last for new onset gout

3-5 days, self limited

how long do sx last for long standing gout

5d to weeks

what are some associated findings for new onset gout

fever, elevated WBC count, elevated inflammatory markers

what are some associated findings for long standing gout

tophi

are patients pain free in intercritical gout

no- affected joints are uncomfortable, swollen

advanced gout is ______ (common/ uncommon) and occurs ____ after initial flare

uncommon >10yrs

2 complications of gout

gouty nephropathy CVD

what are 2 types of gouty nephropathy

uric acid nephrolithiasis interstitial renal disease

uric acid nephrolithiasis depends on

SUA acidity of urine (pH <6 decreases UA solubility) urinary uric acid concentration

uric acid nephrolithiasis can lead to

acute renal failure secondary to ureter obstruction

what is interstitial renal disease/ urate nephropathy

long term deposition of urate crystals in renal parenchyma (micro tophi with giant cell inflammatory reaction)

what are some early signs of interstitial renal disease

proteinuria, inability to concentrate urine

why is hyperuricemia associated with increased risk of CVD

gout is a chronic systemic infalmmatory condition

lab findings in gout

hyperuricemia leukocytosis increased ESR and CRP WBCs in synovial fluid + intracellular MSU crystals present

what is an 100% definitive dx for gout

intracellular MSU crystals found

what is seen on diagnostic imaging for gout?

none for early, maybe some soft tissue swelling intermediate: microtophi on previously affected joints late: bony erosions (punched out marginal erosions)

list 6 differential dx for gout

septic arthritis erosive OA pseudogout trauma cellulitis early polyarticular disease

pseudogout sees a build up of

calcium pyrophosphate dihydrate crystals and calcium hydroxyapatite crystals

which diuretics are associated with gout

thiazide, loop

is ASA 81mg/d still a RF for gout?

yes- any salicylate even if <1g/d

what is the goal of gout tx

cure

goal of pain treatment in gout

>20% in 24hrs >50% at 24hrs

nonpharm tx for gout

avoid contact with affected joints as much as possible rest, ice, elevate dietary: avoid purine and high fructose corn syrup intake

which of the following is true 1. in gout, exercising the joint will often relieve some stiffness and pain 2. gout pain is adequately controlled with NSAIDs + APAP in 80% of pts 3. NHPs may be of benefit in reducing UA 4. dietary restrictions in gout is more effective for chronic prophylaxis than acute

when to initiate tx in acute gout

within 24hrs (ideally 12hrs) of sx onset

T or F: monotx in acute gout is usually effective

when should you consider combination tx in gout flare

severe pain (>7/10) affecting large joints polyarticular if no response to initial monotx (<20% in 24h, <50% > 24h)

what are some combo tx regimens for acute gout

colchicine + NSAID colchicine + oral steroid IA steroid + colchicine or NSAID + oral steroid

colchicine onset

within hrs

colchicine is effective in ___ of pts, most effective if begun within _____ of acute flare

in 2/3 of pts within 12hrs

colchicine at lower doses than flare doses may be used for ____________.

prevention

if colchicine is used at lower doses for prevention, can it still be used for flares

colchicine effect

antiinflammatory

colchicine dosing in acute gout

1.2mg PO stat, then 0.6mg PO 1hr later (within 36hrs of flare onset)

how would you adjust colchicine dose for CrCl <30 or on dialysis

CrCL <30 = no dose adjustment, avoid if used in past 14d dialysis: 0.6mg once daily, avoid if used in last 14d

what is the high dose colchicine regiment

1.2mg PO stat, then 0.6mg PO daily to BID until flare resolved for >24-48hrs (max 6mg/tx course)

what is the max colchicine for tx course

6mg

benefits of low dose over high dose colchicine

less overall AEs less normal and severe diarrhea

colchicine SEs

N/V, cramping, diarrhea myelosuppression, neuromuscular (rhabdo, peripheral neuropathy), liver failure

colchicine interacts with

CYp3A4 and P-gp inhibitors

dose of colchicine if on strong or med CYP3A4 or P-gpi

strong: 0.6mg stat, avoid for 3 d med: 0.6-1.2mg stat, avoid for 3d

how to use NSAIDs for gout fare

high dose for 24-72hrs, then lower doses until sx resolved F1-2d

which NSAIDs are used in gout

indomethacin naproxen celecoxib

which NSAID is preferred for gout

all the same, indomethacin favored from historical perspective

which PO may be used in acute gout

prednisone

which IM CS may be used in acute gout

methylprednisone

efficacy of CS in acute gout

useful when CI to NSAIDs/ colchicine comparable to NSAIDs

when should PO CS be used instead of IA ina cute gout

if >2 joints affected

dose if IA CS depends on

dize of joint

which CS are IA for gout

triamcinolone acetonide, methylprednisolone

when should IA CS be used in gout

if <1-2 large joints are affected

IA CS are usually used in combo with ________ (3) in gout

oral steroids, NSAIDs, or colchicine

anakinra and canakinumab are

IL1 inhibitors invovled in inflammatory response

use of anakinra and canakinumab

consider for tx of severe gout flares refractory or with Ci to other tx

what is the key to chronic gout tx

prevent recurrent attacks

when is gout prophylaxis recommended

=>2 flares/ yr, regardless of SUA =>1 tophus on clinical exam or imaging radiographic damage (any modality) attributable to gout

when is the ideal time to initiate chronic gout tx (urate lowering tx)

may be started during acute flare, as long as effective antiinflammatory management has been instituted

T or F: ongoing prophylactic gout tx may be paused during acute flare tx

F- do not pause

what is important to add when starting ULT

+ antiinflammatory to prevent acute flare during initiation

should we treat to target or treat to avoid sx in gout

either

what is the treat to target approach

target SUA <360 in all pts with gout <300 if tophi or frequent flares until clinical remission is attained

what is the treat to avoid sx approach

do not monitor SUA use a dose of urate lowering tx if necessary that prevents acute flares

nonpharm LT gout tx

pt education on role of uric acid excess, importance of adherence and self tx of future flares weight loss for obese pts screening for CVD and RF stay well hydrated

T or F: gout pts should have a purine restricted diet

F- no RCTS and observational data shows low adherence

what is teh SUA target in pts with severe gout (tophi, freq flares)

<300

what are first line ULT

xanthine oxidase inhibitors - allopurinol and febuxostat

what are second line tx for gout/ if refractory to first line

uricosuric agents (increase renal excretion of uric acid) probenecid, sulfinpyrazone, losartan, fenofibrate

how is adherence for xanthine oxidase inhibitors

low

does allopurinol need tirating

yes- to limit risk of acute flares and serious AEs

how to titrate allopurinol

start at 100mg/d or 50mg/d if CrCL <30 titrate in 50-100mg increments q2-5wks, 3-6mths to reach target dose

allopurinol doses should be divided if > ______ for _____ tolerability

if >300mg/d for GI tolerability

T or F: reduced renal function allopurinol dose adjustments are not evidence based

T or F: drug interactions resulting in allopurinol dose adjustments are evdience based

allopurinol mild AEs

skin rash, GI upset, diarrhea, HA, urticaria, leukopenia

allopurinol serious SEs

allopurinol hypersensitivity sx

sx of allopurinol hypersens sx

rash, hepatitis or interstitial nephritis, fever or eosinophilia or leukocytosis

risks for allopurinol hypersens sx

thiaxides, high initial dose, CKD HLA-B*5801 allele

CrCL required for febuxostat use

>30mL/min

describe febuxostat comp alopurinol in efficacy

not better than allopurinol in preventing gout + higher rate of gout flares

feboxustat should only be used isntead of allopurinol when

serious AE with allopurinol

febuxostat has the same _____ as allopurinol but different _____

same MOA different structure

T or F: febuxostat may be better tolerated than allo ST, but evens out LT

T or F: asymptomatic hyperuricemia should have ULT to prevent flares

F- does not require tx

what are some options for a patient who requires prophylaxis for gout attacks but has previously had a minor rash on allopurinol

allopurinol desensitization for the minor reaction try febuxostat