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PHAR 255 > Gout > Flashcards

Gout Flashcards

1
Q

What is the causing factor for gout?

A

It is a disease resulting from the deposition of monosodium urate:
- Synovial fluids
- Tissues
- Kidney

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2
Q

What is the pathophysiology of gout?

A

Building block of monosodium urate, is uric acid

Uric acid the end product of purine metabolism

Some patients lack the uricase enzyme necessary to metabolize

Overproduction or under-excretion causes hyperuricemia (over 420micromol/L)

Solubility of uric acid decreases with lower temperatures (which is why gout affects joints in the extremities)

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3
Q

Is uric acid rapidly renally excreted?

A

No, it is slowly excreted (prevents crystalization of uric acid in the nephron)

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4
Q

What chronic condition is gout associated with?

A

Obesity (a lot of food rich in fat is metabolized into uric acid)

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5
Q

What are the four clinical phases of gout?

A
  1. Asymptomatic hyperuricemia
  2. Acute gouty arthritis
  3. Intercritical gout
  4. Chronic tophaceous gout
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6
Q

What are the characteristics of asymptomatic hyperuricemia?

A

Elevated uric acid levels (usually more than 420 micromol/L) with no symptoms

Less than 25% will actually develop gout (most do not require drug treatment)

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7
Q

What are some characteristics of acute gouty arthritis?

A

Caused by precipitation of uric acid crystals in joint space (90% of first attacks involve a single joint)

Symptoms:
- Pain
- Erthyema
- Limited range of motion
- Swelling of joint

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8
Q

What are some triggers for acute gouty arthritis?

A

Any activity that can rapidly changing uric acid:
Trauma or surgery
Starvation
Fatty food binge
Dehydration
Drugs (including those that lower urate)

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9
Q

What are some characteristics of intercritical gout?

A

Initial intercritical period can last 2 to 10 years before recurrence (protracted onset of disease)

Best time for patient education and implementation of lifestyle changes

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10
Q

What are some characteristics of chronic tophaceous gout?

A

Tophi are uric acid deposits

Uncommon in most patients

A late complication of hyperuricemia

Can develop on any site (common are the feet and hands)

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11
Q

What are the consequences of chronic tophaceous gout?

A

Joint deformity, destruction, pain
Surrounding tissue damaged
Compresses nerves
Nephrolitiasis and urate nephropathy

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12
Q

What are some complications associated with gout?

A

Nephrolithiasis (Occurs in 10-25% of people with gout, caused by excessive excretion of uric acid)

Urate nephropathy

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13
Q

How is a gout diagnosis made?

A

Baseline lab tests:
- CBC
- Urinalysis and SCr
- BUN
- Serum uric acid levels

Investigate comorbidities and risk factor

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14
Q

What is a way to confrim diagnosis?

A

Analysis of synovial fluid under microscope (visual inspection for uric acid crystals)

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15
Q

What are the goals of treatmenrt for gout?

A
  • Terminate an acute attack
  • Prevent recurrent attacks
  • Prevent long-term complications
  • Treat modiable risk factors
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16
Q

What are the three categories of gout treatment?

A
  • Lifestyle modification (dietary changes)
  • Acute attack drugs (flare management)
  • Preventative drugs (prophylaxis)
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17
Q

When should non-pharmacologic treatment be used alone?

A

Only be implemented during asymptomatic or inter-critical period

  • Regular exercise and weight loss (sufficient in most patients, no significant need to actively cut out purine-rich food)
  • Hydration
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18
Q

What are some examples of purine-rich food that should be avoided in gout patients?

A

Alcohol
Turkey
Veal
Bacon
Liver
High fructose of corn syrup

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19
Q

What are the four options for acute gout flare management?

A
  • NSAIDs
  • Corticosteroids
  • Colchicine
  • Combinations
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20
Q

Is there a clinical reason for why indomethacin is a commonly prescribed NSAID for gout?

A

Not really

It is used because it was first used in gout. It has similar efficacy to other NSAIDs, but increased CNS effects

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21
Q

What are some administration instructions for NSAIDs in gout treatment?

A
  • Use high doses for first 24-72 hours, then find lowest effective dose
  • Usual NSAIDs precautions apply
  • May be used in combination with other acute options
  • Consider adding GI protection (PPIs)
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22
Q

What is a common Naproxen dose for gout flare management?

A

500mg TID from Day 1 to 3

250-500mg BID from Day 4 to 6

Then stop Naproxen (do not abruptly stop Naproxen after Day 3, can cause relapse)

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23
Q

What is the efficacy of NSAIDs in gout treatment?

A

Will significantly reduce symptoms in majority of patients

Speeds resolution

Likely comparable in efficacy to corticosteroids and colchicine

More ADRs than corticosteroids, but less than colchicine

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24
Q

What is the role of corticosteroids in gout flare management?

A

An alternative first-line choice

Prednisone is most commonly used (can be given PO, intra-articular, IV, or IM)

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25
Q

How is prednisone dosed in gout flare management?

A

25-50mg OD for 3-5 days

Short term course for first few flares (no taper required)

For longer course, we taper down due to concerns about relapse when stopping corticosteroids abrupty)

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26
Q

What is the preferred method of administering corticosteroids?

A

Intra-articular steroid injection (especially if only 1 or 2 affected joints)

It works faster and with less side effects than other options (locally acting)

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27
Q

When is corticosteroid therapy cautioned?

A
  • Flare accompanied by fever, chills or other systemic symptoms
  • Diabetic
  • Excessice previous use of steroids
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28
Q

What is the onset of action for colchicine?

A

Should only be initiated if within 24h of flare

May abort attack within 2-3 days

Significant improvement in 24 h

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29
Q

What is the optimal dosing strategy for colchicine?

A

Day 1: Give 1.2mg, then 0.6mg in 1 hour

Following days: 0.6mg BID until resolved (usually takes 7 to 10 days)

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30
Q

Can colchicine be reliably used in patients with renal dysfunction?

A

No, consider alternate flare management

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31
Q

What are some drug interactions associated with colchicine?

A

Main interaction is with 3A4 and PGP inhibitors (toxicity risk)

Statins (may increase level of statins and additive myopathy risk)

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32
Q

How is colchicine dosed in patients on drugs that inhibit 3A4 and PGP?

A

0.6mg, then 0.3mg 1 hour later, do not repeat for 3 days

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33
Q

What is a common side effect associated with colchicine?

A

GI (NVD)
Fatigue

Serious side effects:
- Hematologic abnormalities
- Myopathy/rhabdomyolysis

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34
Q

What are some contraindications for colchicine?

A
  • PGP or 3A4 inhibition in the presence of renal or hepatic impairment
  • Serious GI, hepatic, renal, or cardiac disease
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35
Q

What is the relative tolerability of colchicine?

A

Usually less tolerated vs. other options

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36
Q

What are some good therapeutic combinations for gout flare management?

A
  • Colchicine+NSAIDs
  • Colchicine+Steroids
  • Intra-articular steroid+NSAID or oral steroid or colchicine
37
Q

What gout flare management therapies should be avoided in CKD?

A

Colchicine and NSAIDs

38
Q

What gout flare management therapies should be avoided in CVD?

A

Colchicine and NSAIDs

39
Q

What gout flare managment therapies should be avoided in patients with ulcers/GI issues?

A

NSAIds, steroids, colchicine

40
Q

Which gout flare management therapies should be avoided in diabetes?

A

Avoid steroids

41
Q

What are some qualities that can qualify a patient for gout prophylaxis?

A
  • History of complicated kidney stones or renal insufficiency
  • Every high serum uric acid (more than 800 mircomol/L)
  • Radiographic damage (tophi)
  • more than 1 severe acute attack
  • more than 2 attacks/year (regardless of severity)
42
Q

What are some goals with gout prophylaxis?

A
  • Prevent flares
  • Halt joint destruction and tophi development
  • Slowly lower serum urate to below 300-360 micromol/L
43
Q

Why is slow reduction of uric acid desired in prophylactic therapy?

A

Any rapid changes in uric acid concentration can cause precipitation of crystals (can cause gout attack)

44
Q

Do either colchicine or NSAIDs impact disease mechanism (hyperuricemia) of gout?

A

No, they are more for symptom control

45
Q

What are the hyperuricemic drug classes?

A
  1. Uricosuric
  2. Xanthine oxidase inhibitors
  3. Uricase enzyme (last line)
46
Q

What are the two types of uricosuric agents?

A

Probenecid
Sufinpyrazone

47
Q

What is the mechanism of action for uricosuric drugs?

A

They improve renal clearance of uric acid (useful in patients that are under-excretors)

48
Q

Are uricosuric drugs effective in renal dysfunction?

A

No, once GFR falls below 60mL/min, uricosuric drugs loose efficacy

49
Q

What are some common side effects associated with uricosuric agents?

A
  • Rash
  • GI upset
  • Headache
  • Precipitation of gout flares
50
Q

What are some serious side effects associated with uricosuric agents?

A
  • Nephrolithiasis

Specific to Sulfinpyrazone: bleeds

51
Q

What are some contraindications associated with uricosuric agents?

A
  • Patients on ASA
  • CrCl (less than 60mL/min)
  • History of kidney stones
  • Initiation during an acute flare
52
Q

What are some drug interactions associated with uricosuric drugs?

A
  • NSAIDs
  • Loop diuretics
  • Beta-lactam antibiotics
  • Quinolones
  • Methotrexate
  • Theophylline
  • Sulfonylureas
53
Q

What are some Sulfinpyrazone-specific drug interactions?

A

Due to increased bleed risk

54
Q

What is the relative safety and efficacy of uricosuric agents?

A

Similar efficacy to other hyperuricemic agents

Higher incidence of side effects, so only used when other agents have failed or not tolerated

55
Q

What are some examples of Xanthine Oxidase Inhibitors?

A

Allopurinol
Febuxostat

56
Q

What is the mechanism of action for Xanthine Oxidase Inhibitors?

A

Prevents uric acid synthesis by inhibiting the xanthine oxidase enzyme (useful for over-producers)

57
Q

What are some patient groups that stand to benefit the most from Xanthine Oxidase Inhibitors?

A
  • Over-producers
  • Chronic tophaceous gout
  • History of renal stones or renal dysfunction
  • Frequent or severe attacks
58
Q

What is the onset of action for Xanthine Oxidase Inhibitors?

A

Maximum effect on uric acid reduction in 2 weeks

59
Q

How is Allopurinol dosed and titrated?

A

100mg OD to 800mg/day

Increase dose by 100mg every 4 weeks until uric acid levels are below 360micromol/L

60
Q

Can allopurinol be dosed in renal dysfunction?

A

Yes

  • eGFR 30-60: initial 50mg daily, max 300mg/day
  • eGFR 15-30: Initial 50mg EOD, max 200mg/day
  • eGFR 5-15: Initial 50mg twice weekly, max 100mg/day
  • eGFR under 5: Initial 50mg weekly, max is unknown
61
Q

What are some common side effects associated with allopurinol?

A
  • Rash
  • Pruritus
  • Diarrhea
  • Precipitating gout flare
62
Q

What are some common side effects associated with febuxostat?

A
  • Nausea
  • Arthralgia
  • Rash
  • Precipitating gout flare
63
Q

What is the most significant serious side effect associated with allopurinol?

A

Dermatological hypersensitivity (incidence is less than 1% of all patients)

Associated with morbilliform eruption, erythema multiforme, exfoliative dermatitis

64
Q

What are some types of hypersensitivity reactions associated with allopurinol?

A

Dermatologic
Hematologic
Hepatic toxicity
Renal toxicity

Review slide 61

65
Q

What are some risk factors associated for allopurinol hypersensitivity reactions?

A
  • CKD and CVD (11x risk increase)
  • Too-rapid titration
  • HLA-B*5801 (common in Korean, Thai, and Chinese patients)
  • Concomittent loop/TZD diuretics

Review slide 61

66
Q

What are some serious side effects associated with febuxostat?

A
  • CV risk increase
  • Severe dermal reactions (less than allopurinol)
  • LFT increases
67
Q

What are some precautions for patients starting allopurinol?

A
  • HLA*B5801 genotype (found in higher frequency in Korean, Thai, and Chinese patients)
  • Renal impairment
68
Q

What are some precautions associated with patients starting febuxostat?

A
  • High CV risk patients
  • Hepatic impairment
69
Q

What is the contraindicated drug with febuxostat?

A

Concomitant use with azathioprine or mercaptopurine

70
Q

What are some drug interactions associated with allopurinol?

A
  • ACEi, Loop/TZDs (increased allopurinol hypersensitivity syndrome increased)
  • Azothiprene and mercaptopurine (less severe compared to febuxostat interaction)
  • Amoxicillin
  • Warfarin
71
Q

What xantine oxidase inhibitor is preferred for first drug tried in the class?

A

Allopurinol is initiated first, then substituted with febuxostat if they have issues with Allopurinol (insufficient uric acid reduction, or ADRs)

72
Q

How are xanthine oxidase inhibitors monitored?

A

Every 2-5 weeks during titration, then every 6 months at target (lifelong drugs)

73
Q

What are the two uricase enzymes used in gout treatment?

A
  • Pegloticase
  • Rasburicase (available in Canada)
74
Q

What is the mechanism of action for uricase enzymes?

A

Converts uric acid into allantoin

75
Q

What are some characteristics of uricase enzyme drugs?

A
  • Highly potent agents administered IV every 2-4 weeks
  • Dramatic improvement in flare reduction and tophi in months
  • Reverse complications of debilitating gout
76
Q

What is the role of uricase enzyme therapies in gout treatment?

A
  • Other therapies contraindicated
  • Need for rapid improvement in severe symptoms
  • Numerous flares or tophi
  • Only use until tophi resolves
77
Q

What are some limitations associated with uricase enzyme drugs?

A
  • Antibody development extremely common
  • Infusion reactions common
  • Less tolerated than other options (increased chest pain, severe constipation, more gout flares)
78
Q

For a patient with one or more subcutaneous tophi, should treatment be initiated?

A

Yes, initiate urate lowering therapy

79
Q

For patients with frequent gout flares (more than 2/year), should treatment be initiated?

A

Yes, initiate urate lowering therapy

80
Q

For patients that have experienced gout flares, but are infrequent (less than 2 per year), should treatment be initiated?

A

Depending on patient risk factors (high dietary purine, ACEi & Loop/TZDs, HTN or CVD, high serum urate)

81
Q

For patients after their first gout flare treatment, is treatment indicated?

A

Not at the first flare

82
Q

For high-risk patients (CKD, high serum urate, urolithiasis) that had a single gout flare, is treatment recommended?

A

Depends on individual patient factors

83
Q

For patients with aymptomatic high urate without gout flares or tophi, is treatment reccomended?

A

Despite higher risk with elevated serum urate, we should not initiate urate lowering therapy in these patients

84
Q

Can multiple gout flare treatments be combined and used concurrently?

A

Yes, it is recommended and it should last for 3-6 months

85
Q

Review slide 74-78 for guideline approaches to gout treatment

A
86
Q

What is the first line gout prophylaxis drug class?

A

Xanthine Oxidase Inhibitors

87
Q

What are some good drugs for acute gout flare management in pregnant women?

A

Colchicine and short-course of prednisone are likely safe

88
Q

What are some good drugs for gout prophylaxis in pregnant women?

A

Allopurinol is likely safe

89
Q

Review slide 81 for a review of gout drugs

A

PHAR 255 (15 decks)

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