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Gout Flashcards

1
Q

What is gout?

A

disease resulting from deposition of monosodium urate in synovial fluids, kidney, tissues

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2
Q

What is a building block of monosodium urate?

A

uric acid

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3
Q

Describe uric acid.

A

end product of purine metabolism
no functional role
some lack the uricase enzyme necessary to metabolize
overproduction or underexcretion –> hyperuricemia

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4
Q

Describe hyperuricemia.

A

serum uric acid > 420umol/L
solubility of uric acid decreases with lower temp
precipitation may need a trigger

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5
Q

What can lead to overproduction of uric acid?

A

diet –> overconsumption, diet rich in purines
disease (obesity, hyperTGs)
drugs (diuretics, cytotoxic drugs)

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6
Q

What can lead to underexcretion of uric acid?

A

diseases (CKD, HTN, dehydration)
drugs (diuretics, ACEI/ARB, ASA, alcohol)

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7
Q

Which sex is gout more common in?

A

men
-mostly occurs later in life

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8
Q

What are the four clinical phases of gout?

A

asymptomatic hyperuricemia
acute gouty arthritis
intercritical gout
chronic tophaeus gout

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9
Q

Describe asymptomatic hyperuricemia.

A

elevated uric acid (>420umol/L) but no symptoms
<25% actually develop gout
majority do not require drug treatment
potential consequences:
-gout
-urate nephropathy
-nephrolithiasis
-CKD

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10
Q

What is acute gouty arthritis?

A

caused by precipitation of uric acid crystals in joint space
characterized by sudden onset of:
-pain, erythema, limited ROM, swelling of joint
self-resolving in 7-14 days

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11
Q

How many joints are typically affected by a first gout attack?

A

90% of first attacks involve a single joint

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12
Q

What is the joint involvement frequency?

A

toes > instep > ankle > knee > wrist > fingers

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13
Q

What are some possible triggers of acute gouty arthritis?

A

trauma or surgery
starvation
fatty food binge
dehydration
drugs

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14
Q

What is intercritical gout?

A

asymptomatic period between flares
can last 2-10 years before recurrence
period becomes shorter as disease progresses

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15
Q

When is the best time for patient education and implementation of lifestyle changes in gout?

A

intercritical gout

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16
Q

What is chronic tophaeous gout?

A

tophi are uric acid deposits
uncommon in most
late complication of hyperuricemia

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17
Q

Where does tophaeous gout develop?

A

any site
-most common: hands, feet

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18
Q

What are the consequences of tophaeous gout?

A

joint deformity
surrounding tissue damage
joint destruction and pain
compresses nerves
nephrolithiasis and urate nephropathy

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19
Q

What are some renal complications of gout?

A

nephrolithiasis
-excessive excretion of uric acid
-acidic and highly concentrated urine –> precipitation
urate nephropathy
-acute –> massive precipitation of uric acid crystals in nephrons
-chronic –> microtophi form in kidney

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20
Q

How is gout diagnosed?

A

primarily based on symptoms
baseline labs: CBC, SCr, BUN, urinalysis, serum uric acid
Xray typically not useful
may confirm by analysis of synovial fluid under microscope
point system

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21
Q

What are the goals of therapy for gout?

A

terminate an acute attack
prevent recurrent attacks
prevent long-term complications
treat modifiable risk factors

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22
Q

What are the three components of gout treatment?

A

lifestyle modification
acute attack drugs
preventative drugs

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23
Q

When should non-pharm treatment be implemented for gout?

A

during the asymptomatic or intercritical period

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24
Q

What are non-pharm strategies for gout?

A

exercise and weight loss
hydration
RICE (without the compression)
diet (limit calories in general)

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25
What are some foods to avoid in gout?
turkey bacon veal liver beer high fructose or corn syrup foods
26
What are the treatment options for an acute gout flare?
NSAIDs steroids colchicine
27
What is a common first-line choice for an acute gout flare?
NSAIDs
28
Which NSAIDs can be used for an acute gout flare?
any NSAID can be used -HC indication: naproxen, ibuprofen, ketoprofen, indomethacin (not special for gout), celecoxib
29
How are NSAIDs dosed for an acute gout flare?
high dose for first 24-72h then find LED -use 2-3 days post improvement
30
True or false: NSAIDs cannot be combined with other acute options during a gout flare
false they can be combined
31
Describe the efficacy and safety of NSAIDs for an acute gout flare.
significantly reduce symptoms in majority speeds resolution comparable efficacy to steroids and colchicine more ADRs than steroids, less than colchicine
32
What is an alternative first-line option for an acute gout flare, asides from NSAIDs?
corticosteroids
33
Which corticosteroid is commonly common used for acute gout flares? How is it dosed?
prednisone 25-50mg OD x 3-5 days
34
Which routes of admin are available for corticosteroids during an acute gout flare?
po intra-articular IM IV
35
What are the tapering recommendations for corticosteroids and gout?
short term for first few flares: no taper concomitant anti-infl or urate lowering therapy: unlikely need taper long course: taper over 1-2 weeks multiple-flare hx or short intercritical period: taper
36
When are intra-articular steroids the preferred option for an acute gout flare?
access to experienced physician and only 1-2 affected joints
37
What is the benefit of intra-articular steroids for acute gout flare?
works faster and less side effects than other options
38
How many times can a joint undergo an intra-articular injection per year?
4x/year
39
What is the use of parenteral steroids for acute gout flare?
reserved for severe flares or cant take oral meds
40
When should you be cautious with corticosteroid use in an acute gout flare?
flare accompanied by fever, chills, other systemic sx diabetic excessive previous use of steroids
41
Describe the efficacy and safety of corticosteroids for an acute gout flare.
as efficacious as NSAIDs and colchicine likely best tolerated serious AE unlikely with episodic use
42
Which acute option has considerable ADR and toxicity?
colchicine
43
What is the MOA of colchicine?
inhibits WBC motility in joint space --> reduces inflammation
44
When should colchicine be initiated for an acute gout flare?
within 24h of flare
45
What is the onset for colchicine?
aborts attack within 2-3 days significant improvement within 24h
46
What is the optimal dosing for colchicine?
day 1: 1.2mg now, then 0..6mg in 1h (1.8mg total) -then 0.6mg OD-BID until resolved (~7-10d) close second: 0.6mg BID x 1-3d, then 0.6mg OD until resolved
47
When do we adjust the dose for colchicine?
renal impairment -consider alternative acute option hepatic impairment -consider alt acute option if severe impairment moderate 3A4 or P-gp inhibitor -use lower dose -CI if renal/hepatic impairment
48
What are the common adverse effects of colchicine?
NVD fatigue
49
What are the serious adverse effects of colchicine?
hematologic abnormalities myopathy/rhabdo
50
What are the drug interactions of colchicine?
increased statin levels (myopathy risk) main risk: 3A4 and P-gp inhibitors -clarithromycin, grapefruit juice, non-DHP CCB, azoles
51
What are the contraindications of colchicine?
3A4 or P-gp inhibitor with renal/hepatic impairment severe GI, renal, hepatic, cardiac disease
52
Describe the efficacy and safety of colchicine.
similar efficacy to NSAIDs or steroids, perhaps faster excellent safety when used in low-dose regimens less tolerated than other options
53
When is combination therapy used for an acute gout flare?
severe flares or unresponsive to monotherapy
54
What are the combination options for an acute gout flare?
NSAID + colchicine steroid + colchicine intra-articular steroid + NSAID/oral steroid/colchicine
55
Who are the candidates for gout prophylaxis?
history of complicated kidney stones or renal insufficiency radiographic damage, tophi very high uric acid (>800umol/L) even if asymptomatic >1 severe acute attack >2 attacks/year
56
Who does not need gout prophylaxis?
mild first episode infrequent flares and adequate response to acute therapy infrequent flares and low serum uric acid asymptomatic hyperuricemia < 800umol/L and no risk factors
57
What are the goals for gout prophylaxis?
prevent flares halt joint destruction and tophi development SLOWLY return serum urate < 300-360 umol/L
58
How do we initiate therapy with the drugs used for gout prophylaxis?
initiate at low doses and titrate slowly
58
What is the role of NSAIDs or colchicine in gout prophylaxis?
prevent flare during initiation of other prophylactic agents -does not correct hyperuricemia or prevent tophi
58
What are the options for gout prophylaxis?
colchicine or NSAIDs hyperuricemic drugs: -uricosuric drugs -xanthine oxidase inhibitors -uricase enzymes
59
What are the doses of NSAIDs and colchicine for gout prophylaxis?
indomethacin 25mg BID naproxen 250mg BID colchicine 0.6mg 3x/wk; up to 0.6mg BID
60
How long are NSAIDs or colchicine used for gout prophylaxis?
3-6 months
61
What are examples of uricosuric agents?
probenecid sulfinpyrazone
62
What is the MOA of uricosuric agents?
increase renal clearance of uric acid
63
What is the role of uricosuric agents?
under excretor of uric acid -require good kidney health for efficacy
64
What is the onset of uricosuric agents?
both begin lowering serum urate immediately
65
What is the dosing and administration for uricosuric agents?
start low and titrate slowly ensure adequate hydration
66
What are the common adverse effects of uricosuric agents?
GI upset rash headache precipitation of gout flares
67
What are the serious adverse effects of uricosuric agents?
nephrolithiasis bleeds (sulfinpyrazone)
68
What are contraindications of uricosuric agents?
pts on ASA CrCl < 60ml/min initiation during an acute flare history of kidney stones
69
What are the drug interactions of uricosuric agents?
increased [ ] of drugs relying on renal excretion sulfinpyrazone: antiplatelets, anticoag, phenytoin
70
Describe the efficacy of uricosuric agents.
similar efficacy to other hyperuricemic agents higher AE rate only use when other agents failed/intolerated
71
What are examples of xanthine oxidase inhibitors?
allopurinol febuxostat
72
What is the MOA of xanthine oxidase inhibitors?
prevent uric acid synthesis by inhibiting xanthine oxidase
73
Which populations are xanthine oxidase inhibitors best used in?
frequent or severe attacks chronic tophaceous gout history of kidney stones or renal dysfunction over producers
74
What is the onset of xanthine oxidase inhibitors?
max effect on uric acid reduction in 2 weeks
75
What are the dosing principles of the xanthine oxidase inhibitors?
start low and titrate slowly q4wks can be used in renal impairment target 300-360 umol/L
76
What are the common adverse effects of the xanthine oxidase inhibitors?
allopurinol: -rash -pruritis -diarrhea -precipitating gout flare (use NSAID or colchicine to lower risk) febuxostat: -rash -nausea -arthralgia -precipitating gout flare (use NSAID or colchicine to lower risk)
77
What are the serious adverse effects of xanthine oxidase inhibitors?
allopurinol: allopurinol hypersensitivity syndrome -dermatologic, hematologic, renal, hepatic febuxostat: CV risk, dermal rxns, LFT increase
78
What are the risk factors for allopurinol hypersensitivity syndrome?
CKD and CVD too-rapid titration HLA-A*5801 genotype loop/thiazide diuretic
79
What are the precautions for xanthine oxidase inhibitors?
allopurinol: -HLA-B*5801 genotype, renal impairment febuxostat: -CV risk pts, hepatic impairment
80
What are contraindications of xanthine oxidase inhibitors?
allopurinol: none febuxostat: use with azathioprine or mercaptopurine
81
What are the drug interactions of the xanthine oxidase inhibitors?
allopurinol: -no enzyme influence -ACEI (increased risk of hypersensitivity syndrome) -diuretics (increased risk of hypersensitivity syndrome) -warfarin -amoxicillin -azathioprine and mercaptopurine febuxostat: -no enzyme influence -azathioprine and mercaptopurine
82
Compare febuxostat and allopurinol.
febuxostat associated with precipitating more flares febuxostat may achieve target serum urate more febuxostat may reduce tophi more differences in common and serious ADRs
83
When do we use febuxostat?
allopurinol fails to achieve serum urate target hypersensitive to allopurinol
84
What are the monitoring parameters for the xanthine oxidase inhibitors?
serum urate q2-5wks during titration, q6mo at target LFTs (febuxostat)
85
What are examples of uricase enzymes?
pegloticase rasburicase
86
What is the MOA of uricase enzymes?
converts uric acid into allantoin
87
What are the benefits of the uricase enzymes?
dramatic improvement in flares and tophi in months reverse complications of debilitating gout *highly potent, given IV q2-4wks*
88
What are the indications for uricase enzymes?
other therapies CI need for rapid improvement in severe symptoms numerous flares or tophi *guidelines: severe gout, others failed, only use until tophi resolves*
89
What are the limitations of uricase enzymes?
antibody development infusion reactions less tolerated than other options
90
Based on a guideline approach, who should be placed on urate lowering therapy?
> 1 subcutaneous tophi >1 flare but have infrequent flares (< 2/yr) first flare and CKD, SU >500mmol/L, urolithiasis AGAINST: first flare, asymptomatic hyperuricemia
91
Based on a guideline approach, which ULT should be used?
allopurinol at low dose and titrating concomitant anti-inflammatory agents for 3-6 months
92
Based on a guideline approach, what are the primary treatment targets?
treat to target SU continuing indefinitely > stopping ULT
93
Based on a guideline approach, when do we consider switching ULT?
continued frequent flares/not at SU target despite maximum tolerated dose
94
Based on a guideline approach, what is the management for flares?
colchicine, NSAID, steroid = 1st line -low dose colchicine > high dose colchicine
95
Describe gout management in pregnancy.
acute flares: -avoid NSAIDs -colchicine and short course prednisone likely safe prophylaxis: -allopurinol likely safe -limited data for febuxostat=avoid lactation: -ibuprofen, prednisone, allopurinol are safe

PHAR255 (24 decks)

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