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255B > Gout > Flashcards

Gout Flashcards

1
Q

What should you know about uric acid?

A

end product of purine metabolism
has no functional role
some lack the uricase enzyme necessary to metabolise
overproduction or under-excretion (hyperuricemia)

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2
Q

Definition of hyperuricemia

A

a serum uric acid concentration over 420 umol/l
solubility of uric acid decreases with lower temperatures

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3
Q

How to figure out the patient overproducing or under-excreting?

A

place person on purine free diet for 3-5 days
- measure amount of uric acid in urine in 24 hours
on a regular diet
- excretion of > 1000 mg/24h = overproducer
less then 1000 mg/24 h = underexcretion (assuming high serum uric acid)

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4
Q

List the four clinical phases of gout

A

Asymptomatic hyperuricemia

Acute gouty arthritis

Intercritical gout

Chronic tophaceous gout

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5
Q

Describe asymptomatic hyperuricemia

A

elevated uric acid levels (+420 umol/l) with no sx
majority do not require drug tx

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6
Q

Describe acute gouty arthritis

A

caused by precipiation of uric acid crystals in joint space
- immune system involvement -> vasodilation -> increased permeability

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7
Q

List some characterization of acute gouty arthritis

A

pain
erythema
limited range of motion
swelling of joint

self-resolves in 7-14 days

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8
Q

List some possible triggers acute gouty arthritis

A

trauma or surgery
starvation
fatty food binge
dehydration
drugs - including urate-lowering therapy

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9
Q

Describe intercritical gout

A

asymptomatic period between flares
initial intercritical period can last 2-10 years before recurrence

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10
Q

Describe chronic tophaceous gout

A

tophi are uric acid deposits
uncommon in most
late complication of hyperuricemia
can develop at any site

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11
Q

What is the difference between RA and gout?

A

will look like RA but will be very painful and it will take years to decrease

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12
Q

Describe nephrolithiasis

A

Occurs in 10-25% of people with gout
Caused by excessive excretion of uric acid

Acidic and highly concentrated urine  precipitation

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13
Q

Describe urate nephropathy

A

Acute - massive precipitation of uric acid crystals in nephrons
Chronic - microtophi form in kidneys

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14
Q

What are some factors in the point scale for the diagnosis of gout?

A

Male (2)
Previous similar flare (2)
Rapid onset within one day (0.5)
Joint redness (1)
Toe involved (2.5)
Presence of HTN or CVD (1.5)
High serum urate (3.5)

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15
Q

List some of the goals of therapy of gout

A

Terminate an acute attack
Prevent recurrent attacks
Prevent long-term complications
Treat modifiable risk factors

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16
Q

What is the main options for acute gout flare?

A

NSAIDs
corticosteroids
colchicine
combo

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17
Q

What should you know abou NSAID use in acute gout flares?

A

high doses for first 24-72 h, then find lowest effective dose
usual NSAIDs precautions apply
may be used in combination with other acute options
consider adding GI protection (maybe add PPIs)

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18
Q

When should you stop the NSAID after an acute gout flare?

A

only stop nsaid after 2-3 sx free days

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19
Q

Efficacy and safety for NSAIDs during acute got flare

A

will significantly reduce symptoms in majority of patients
Speeds resolution
Likely comparable in efficacy to corticosteroids and colchicine
More ADR than corticosteroids, but less than colchicine

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20
Q

What should you know about corticosteroids use for acute gout flare?

A

an alternative first line choice
prednisone most commonly used
can be given PO, intra-articular, IV or IM
limited by how often should be used

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21
Q

What should you know about intra-articular steroid injection using for acute gout flare?

A

Preferred option if access to experienced physician and only 1-2 affected joints
Works faster and with less side-effects than other options
Limit to one joint 4x/year

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22
Q

List some efficacy and safety for steroids in acute gout flares?

A

As efficacious as NSAIDs and colchicine
Likely the best tolerated
Serious side-effects unlikely with episodic use

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23
Q

What are some cautions to think about for steroids and acute got flares?

A

Flare accompanied by fever, chills or other systemic symptoms
Diabetic
Excessive previous use of steroids

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24
Q

MOA of colchicine

A

Inhibits WBC motility in joint space  reduces inflammation
May also prevent deposition of urate in synovial fluid

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25
Q

Onset of effect for colchicine

A

Should only be initiated if within 24h of flare
May abort attack within 2-3 days
Significant improvement in 24h

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26
Q

What is the optimal dosing for colchicine?

A

Day 1: Give 1.2mg, then 0.6mg in 1 hour (1.8mg total)
Continue with 0.6mg OD or BID thereafter until resolved (~7-10 days)

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27
Q

Do you have dosing adjustments for renal impairment and colchicine?

A

Yes for anything under 80 ml/min

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28
Q

DDI for colchicine

A

Taking moderate or strong 3A4 OR P-GP inhibitors
If concurrent renal / hepatic impairment  contraindicated
Otherwise, use lower dose regimen:
0.6mg, then 0.3mg 1h later; do not repeat for 3 days

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29
Q

Common S/e of colchicine

A

GI -> nausea, vomiting, diarrhea
fatigue

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30
Q

Serious s/e of colchicine

A

hematologic abnormalities
myopathy / rhabdomyolysis

31
Q

CI for colchicine

A

Pgp or 3A4 inhibition in the presence of renal or hepatic impairment
Serious GI, hepatic, renal or cardiac disease

32
Q

Efficacy and safety for colchicine

A

No rigorous comparative trials available
Likely similar efficacy to NSAIDs or steroids, perhaps faster onset
If used in low-dose regimens in proper patients, excellent safety
Usually less tolerated vs. other options

33
Q

List some combo options for acute gout flare

A

Colchicine + NSAID
Colchicine + Steroids
Intra-articular steroid + NSAID or oral steroid or colchicine

NOT NSAID and STEROIDS

34
Q

What to consider when selecting medication for acute gout flare?

A

Patient comorbidities (e.g. CKD, CVD, ulcers/GI issues, diabetes)
Other medications
Gout history
Total flare number
Rate of recurrence
Previous medication use experience
Duration of flare
Number of affected joints

35
Q

Candidates for gout prophylaxis

A

History of complicated kidney stones or renal insufficiency (<60ml/min)
Very high serum uric acid (>800 umol/L) even if asymptomatic
Radiographic damage, tophi
>1 severe acute attack
>2 attacks/year

36
Q

Patients who do not need prophylaxis for gout

A

Mild first episode
Infrequent flares and adequate response to acute therapy
Infrequent flares and low serum uric acid
Asymptomatic hyperuricemia if <800 umol/L and no significant risk factors

37
Q

List some goals for gout prophylaxis

A

Prevent flares
Halt joint destruction and tophi development
Slowly lower serum urate to <300-360 umol/L

38
Q

What should you know about colchicine or NSAIDs as ppx for gout?

A

Main role: prevent flares during initiation of other prophylactic agents
Does not correct hyperuricemia or prevent tophi
typical duration is 3-6 months - depends on serum urate values

39
Q

List some hyperuricemic drugs

A

Probenecid (not currently available in Canada)
Sulfinpyrazone

40
Q

Onset of uricosuric agents

A

both being lowering serum urate immediately

41
Q

Common s/e of uricosuric agents

A

Rash
GI upset
Headache
Precipitation of gout flares

42
Q

Serious s/e for uricosuric agents

A

Nephrolithiasis (kidney stones)
Sulfinpyrazone: bleeds

43
Q

CI for uricosuric agents

A

Patients on ASA -> blocks it from working
CrCl <60ml/min
History of kidney stones
Initiation during an acute flare

44
Q

DDI for uricosuric agents

A

Both increase concentration of drugs primarily relying on renal excretion
NSAIDs
Loop diuretics
Beta-lactam antibiotics
Quinolones
Methotrexate
Theophylline
Sulfonylureas

45
Q

Efficacy data for uricosuric agents

A

Similar efficacy to other hyperuricemic agents
~1/3 of patients achieve target uric acid levels
Higher rates of common / serious side effects
Only used when other agents failed or not tolerated

46
Q

List some xanthine oxidase inhibitors

A

allopurinol
febuxostat

47
Q

MOA of XOI

A

Prevents uric acid synthesis by inhibiting the xanthineoxidase enzyme

48
Q

Best to use XOI in …

A

Over-producers
Chronic tophaceous gout
History of renal stones or renal dysfunction
Frequent or severe attacks

49
Q

Onset of XOI

A

max effect on uric acid reduction in 2 weeks

50
Q

Basic dosing info for XOI

A

increase allopurinol 100 mg q4w
can be used in renal

51
Q

Common s/e of allopurinol

A

Rash
Pruritus
Diarrhea
Precipitating gout flare

52
Q

Common s/e febuxostat

A

Nausea
Arthralgia
Rash
Precipitating gout flare

53
Q

What should be initiated with XOI for PPX for gout?

A

start an NSAID or colchicine alongside to reduce the chance of a flare (often counsel for them to use naproxen OTC if not rx for a couple of weeks)

54
Q

Serious s/e for allopurinol

A

Dermatologic: morbilliform eruption, erythema multiforme, exfoliative dermatitis
Hematologic: eosinophilia, agranulocytosis, aplastic anemia, thrombocytopenia
Hepatic toxicity
Renal toxicity

55
Q

List some risk factors that increase serious s/e for allopurinol

A

CKD and CVD (11x risk increase)
Too-rapid titration
HLA-B*5801 genotype
Concomitant loop/thiazide diuretics increase risk
Incidence of ~0.1-0.4% or 1 to 4 per 1000

56
Q

Serious s/e for febuxostat

A

Cardiovascular risk increase
Severe dermal reactions (< allopurinol)
LFT increases

57
Q

Precautions for allopurinol

A

HLA-B* 5801 genotype
renal impairment

58
Q

Precautions for febuxostat

A

High CV risk patients
Hepatic impairment

59
Q

CI for allopurinol

A

none

60
Q

CI for febuxostat

A

Concomitant use with azathioprine or mercaptopurine

61
Q

Main DDI to know for allopurinol

A

ACE inhibitor - allopurinol hypersensitivity syndrome increased
loop/thiazide diuretics - allopurinol hypersensitivity syndrome increased

62
Q

DDI with febuxostat

A

Concomitant use with azathioprine or mercaptopurine

63
Q

Differences b/w allopurinol vs febuxostat

A

Febuxostat associated with precipitating more gout flares
Febuxostat may achieve target serum urate more than allopurinol
Febuxostat may reduce tophi more than allopurinol (minor)
Some differences in common and serious ADRs

64
Q

Monitoring with XOI

A

Serum urate
every 2-5 weeks during titration
Every 6 months at target

Febuxostat: Additional LFTs

65
Q

List the uricase enzyme

A

Includes:
Pegloticase – US only
Rasburicase – now available in Canada

66
Q

MOA for uricase enzyme

A

converts uric acid into allantoin

67
Q

What should you know about uricase enzyme?

A

Highly potent agents administered IV every 2-4 weeks

Dramatic improvement in flare reduction and tophi in months

Reverse complications of debilitating gout

68
Q

Indications to use uricase enzyme for gout ppx

A

Indications:
Other therapies contraindicated
Need for rapid improvement in severe symptoms
Numerous flares or tophi

69
Q

Limitations for uricase enzymes

A

Antibody development extremely common
Infusion reactions common
Less tolerated than other options:
Chest pain
Severe constipation/nausea/vomiting
Precipitates gout flares more often

70
Q

When do the guidelines suggest using uricase enzyme?

A

use only if severe gout, if other options failed, and only use until tophi resolves

71
Q

List some practical tips for tx for gout

A

Don’t worry about underexcreter vs. over-producer

Watch for patients using several courses of acute flare therapy

Have an early discussion about prophylactic therapy

Watch for optimal dosing, timing, and titration

72
Q

Pregnancy options for acute gout flares

A

Generally avoid NSAIDs in 1st and 3rd trimester
Colchicine and short-courses of prednisone are likely safe

73
Q

Pregnancy options for ppx for gout

A

Allopurinol likely safe
Febuxostat – limited data  avoid

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