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443-SRH and MSK > Gout > Flashcards

Gout Flashcards

1
Q

what is gout?

A

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

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2
Q

what is hyperuricemia

A

elevated serum urate concentration

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3
Q

what is acute arthritis

A

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

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4
Q

what are tophi

A

deposits of monosodium urate crystals in tissues in and around joints

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5
Q

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

A

1

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6
Q

what is the peak age for gout diagnosis

A

40-50 in males
>60 in females

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7
Q

is there a genetic link to gout?

A

yes

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8
Q

in asymptomatic hyperuricemia, ____ go on to develop acute gout

A

25%

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9
Q

what are the 4 steps in the course of gout illness

A

asymptomatic hyperuricemia
acute gouty arthritis
intercritical gout
advanced gout

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10
Q

what enzyme is responsible for the production of uric acid

A

xanthine oxidase

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11
Q

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

A

uricase

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12
Q

causes of primary gout (overproduction)

A

idiopathic
genetic enzyme abnormalities

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13
Q

what causes primary gout with underexcretion of UA

A

idiopathic

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14
Q

what causes secondary overproduction of UA

A

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

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15
Q

what causes secondary underexcretion of UA

A

decreased renal function
metabolic acidosis
dehydration

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16
Q

list some diet related factors that change SUA

A

meat, seafood intake
alcohol
high fructose content

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17
Q

drug related factors that change SUA

A

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

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18
Q

disease related factors that change SUA

A

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

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19
Q

what are 3 factors that lower the risk of gout

A

dairy
coffee (including decaf)
vit C

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20
Q

acute gouty arthritis is usually ____ and resolves ___________ within ______

A

usually monoarticular
resolves spontaneously in 7-10d

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21
Q

what is the clinical presentation of acute gout

A

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

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22
Q

presumptive diagnosis of gout if:

A

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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23
Q

what is intercritical gout

A

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

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24
Q

what is the typical patient of new onset gout

A

hyperuricemia, postmenopausal women, men >30yrs

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25
Q

what is the typical patient fo rlong standing fout

A

elderly men or women

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26
Q

how long do sx usually last for new onset gout

A

3-5 days, self limited

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27
Q

how long do sx last for long standing gout

A

5d to weeks

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28
Q

what are some associated findings for new onset gout

A

fever, elevated WBC count, elevated inflammatory markers

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29
Q

what are some associated findings for long standing gout

A

tophi

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30
Q

are patients pain free in intercritical gout

A

no- affected joints are uncomfortable, swollen

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31
Q

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

A

uncommon
>10yrs

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32
Q

2 complications of gout

A

gouty nephropathy
CVD

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33
Q

what are 2 types of gouty nephropathy

A

uric acid nephrolithiasis
interstitial renal disease

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34
Q

uric acid nephrolithiasis depends on

A

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

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35
Q

uric acid nephrolithiasis can lead to

A

acute renal failure secondary to ureter obstruction

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36
Q

what is interstitial renal disease/ urate nephropathy

A

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

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37
Q

what are some early signs of interstitial renal disease

A

proteinuria, inability to concentrate urine

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38
Q

why is hyperuricemia associated with increased risk of CVD

A

gout is a chronic systemic infalmmatory condition

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39
Q

lab findings in gout

A

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

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40
Q

what is an 100% definitive dx for gout

A

intracellular MSU crystals found

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41
Q

what is seen on diagnostic imaging for gout?

A

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

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42
Q

list 6 differential dx for gout

A

septic arthritis
erosive OA
pseudogout
trauma
cellulitis
early polyarticular disease

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43
Q

pseudogout sees a build up of

A

calcium pyrophosphate dihydrate crystals and calcium hydroxyapatite crystals

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44
Q

which diuretics are associated with gout

A

thiazide, loop

45
Q

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

A

yes- any salicylate even if <1g/d

46
Q

what is the goal of gout tx

A

cure

47
Q

goal of pain treatment in gout

A

> 20% in 24hrs
50% at 24hrs

48
Q

nonpharm tx for gout

A

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

49
Q

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

A

4

50
Q

when to initiate tx in acute gout

A

within 24hrs (ideally 12hrs) of sx onset

51
Q

T or F: monotx in acute gout is usually effective

A

T

52
Q

when should you consider combination tx in gout flare

A

severe pain (>7/10)
affecting large joints
polyarticular

if no response to initial monotx (<20% in 24h, <50% > 24h)

53
Q

what are some combo tx regimens for acute gout

A

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

54
Q

colchicine onset

A

within hrs

55
Q

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

A

in 2/3 of pts
within 12hrs

56
Q

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

A

prevention

57
Q

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

A

no

58
Q

colchicine effect

A

antiinflammatory

59
Q

colchicine dosing in acute gout

A

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

60
Q

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

A

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

61
Q

what is the high dose colchicine regiment

A

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

62
Q

what is the max colchicine for tx course

A

6mg

63
Q

benefits of low dose over high dose colchicine

A

less overall AEs
less normal and severe diarrhea

64
Q

colchicine SEs

A

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

65
Q

colchicine interacts with

A

CYp3A4 and P-gp inhibitors

66
Q

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

A

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

67
Q

how to use NSAIDs for gout fare

A

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

68
Q

which NSAIDs are used in gout

A

indomethacin
naproxen
celecoxib

69
Q

which NSAID is preferred for gout

A

all the same, indomethacin favored from historical perspective

70
Q

which PO may be used in acute gout

A

prednisone

71
Q

which IM CS may be used in acute gout

A

methylprednisone

72
Q

efficacy of CS in acute gout

A

useful when CI to NSAIDs/ colchicine
comparable to NSAIDs

73
Q

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

A

if >2 joints affected

74
Q

dose if IA CS depends on

A

dize of joint

75
Q

which CS are IA for gout

A

triamcinolone acetonide, methylprednisolone

76
Q

when should IA CS be used in gout

A

if <1-2 large joints are affected

77
Q

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

A

oral steroids, NSAIDs, or colchicine

78
Q

anakinra and canakinumab are

A

IL1 inhibitors invovled in inflammatory response

79
Q

use of anakinra and canakinumab

A

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

80
Q

what is the key to chronic gout tx

A

prevent recurrent attacks

81
Q

when is gout prophylaxis recommended

A

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

82
Q

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

A

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

83
Q

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

A

F- do not pause

84
Q

what is important to add when starting ULT

A

+ antiinflammatory to prevent acute flare during initiation

85
Q

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

A

either

86
Q

what is the treat to target approach

A

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

87
Q

what is the treat to avoid sx approach

A

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

88
Q

nonpharm LT gout tx

A

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

89
Q

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

A

F- no RCTS and observational data shows low adherence

90
Q

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

A

<300

91
Q

what are first line ULT

A

xanthine oxidase inhibitors - allopurinol and febuxostat

92
Q

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

A

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

93
Q

how is adherence for xanthine oxidase inhibitors

A

low

94
Q

does allopurinol need tirating

A

yes- to limit risk of acute flares and serious AEs

95
Q

how to titrate allopurinol

A

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

96
Q

allopurinol doses should be divided if > ______ for _____ tolerability

A

if >300mg/d for GI tolerability

97
Q

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

A

T

98
Q

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

A

T

99
Q

allopurinol mild AEs

A

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

100
Q

allopurinol serious SEs

A

allopurinol hypersensitivity sx

101
Q

sx of allopurinol hypersens sx

A

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

102
Q

risks for allopurinol hypersens sx

A

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

103
Q

CrCL required for febuxostat use

A

> 30mL/min

104
Q

describe febuxostat comp alopurinol in efficacy

A

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

105
Q

feboxustat should only be used isntead of allopurinol when

A

serious AE with allopurinol

106
Q

febuxostat has the same _____ as allopurinol but different _____

A

same MOA
different structure

107
Q

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

A

T

108
Q

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

A

F- does not require tx

109
Q

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

A

allopurinol desensitization for the minor reaction
try febuxostat

443-SRH and MSK (24 decks)

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