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Year 3 - Clinical (Winter) > 24 - Gout > Flashcards

24 - Gout Flashcards

1
Q

Definition of gout

A

Group of heterogeneous diseases characterized by arthropathy resulting from the deposition of urate crystals in and around the joints

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2
Q

Modifiable risk factors for gout

A
  • Hyperuricemia
  • Hypertension, obesity, diabetes
  • Alcohol consumption (binge drinking can precipitate attacks in those susceptible)
  • High purine intake
  • Drugs
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3
Q

Non-modifiable risk factors for gout

A
  • Chronic kidney disease
  • Male gender
  • Age
  • Genetics, family hx
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4
Q

What is hyperuricemia and how can it occur?

A
  • Definition = serum uric acid > 480 umol/L in males or > 420 umol/L in females
  • Etiology = overproduction and/or underexcretion
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5
Q

How is uric acid produced?

A
  • Dietary intake, breakdown of tissue nucleic acids, and de novo synthesis => purines (guanine, adenine)
  • Degradation of purines => uric acid
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6
Q

Do the majority of gout px have uric acid overproduction or underexcretion?

A

Underexcretion

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7
Q

What can cause uric acid overproduction?

A
  • Diet
  • Tissue/cell breakdown
  • Metabolic derangement
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8
Q

What can cause uric acid underexcretion?

A

Renal abnormalities (67% of uric acid excreted by kidneys)

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9
Q

Describe renal excretion of uric acid

A
  • 100% of uric acid enters glomerulus
  • Majority is reabsorbed, leaving 0-2% in the proximal tubule
  • Then some is secreted back into proximal tubule and reabsorbed again leaving 8-12% to be excreted
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10
Q

Factors altering renal excretion of uric acid

A
  • Decreased GFR
  • Decreased active secretion of uric acid (ex: salicylates < 2 g/day, loop and thiazide diuretics, acute EtOH)
  • Increased post-secretory resorption (ex: dehydration, high dose ASA)
  • Undefined (ex: HTN, hyperparathyroidism, cyclosporine)
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11
Q

What is monosodium urate (MSU)?

A
  • Ionized form of uric acid; most common form of uric acid in the blood?
  • Limited solubility in plasma (even lower solubility at lower temps and the toes are some of the coldest parts of the body)
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12
Q

Pathophysiology of gout

A

Saturation of synovial fluid w/ uric acid -> crystal formation -> activation of inflammatory response -> leukocytes and macrophages -> proteolytic enzymes, prostaglandins, leukotrienes; activation of clotting, kininogen, plasminogen and complement cascades -> damage to articular cartilage and injury to soft tissue

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13
Q

Clinical characteristics of acute gouty arthritis

A
  • Sudden onset of warmth, swelling, erythema, and unbearable joint pain
  • 50% of first attacks occur at metatarsophalangeal joint of the great toe only
  • 90% will have involvement of this site sometime during their disease
  • 10% of first attacks involve 2 or more joints
  • Systemic sx such as fever, chills & malaise may be present
  • Untreated sx last 3-14 days before spontaneous recovery
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14
Q

Joints affected in gout

A
  • Most common = toe, instep, ankle
  • Medium prevalence = heel, knee, wrist
  • Low prevalence = finger, elbow
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15
Q

Precipitating factors of gout

A
  • Stress or trauma at the joint
  • Alcohol (binge drinking)
  • Infection, surgery
  • Rapid lowering of serum uric acid
  • Drugs that increase uric acid
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16
Q

Diagnosis of acute gout

A

Demonstration of sodium urate crystals in affected joint (take a sample of the fluid from the affected joint and analyze for sodium urate crystals)

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17
Q

What are intercritical periods?

A
  • Periods between attacks
  • 2nd attack w/in 6 months to 2 years
  • W/ subsequent attacks, intercritical periods become shorter
  • Attacks become polyarticular, more severe and longer lasting
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18
Q

Chronic complications of gout

A
  • Nephrolithiasis
  • Gouty nephropathy (acute uric acid nephropathy or chronic urate nephropathy)
  • Tophi formation
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19
Q

What is chronic tophaceous gout?

A
  • Chronic urate deposits in cartilage, tendons, synovial membranes
  • Common sites = toe, fingers, wrists, ears, knees, achilles tendon
  • Occur when intercritical periods no longer pain free (10 years of acute intermittent gout)
  • 50-70% of px if hyperuricemic therapy not initiated
  • W/ the use of hypouricemic agents, prevalence decreases to 3-21%
  • Joints persistently uncomfortable and swollen
  • Acute gout attacks continue to occur
20
Q

Gout tx goals

A
  • Relieve pain and inflammation w/in 48 h of an acute attack
  • Complete resolution of sx in 7 days
  • Reduce uric acid levels to < 360 umol/L
  • Prevent recurrent attacks of gouty arthritis
  • Prevent chronic complications of gout
21
Q

Gout management approach

A
  1. Treat acute flare rapidly w/ an anti-inflammatory agent
  2. Initiate urate-lowering therapy to achieve serum urate < 6 mg/dL; use concomitant anti-inflammatory prophylaxis for up to 6 months to prevent mobilization flares
  3. Continue urate-lowering therapy to control flares and avoid continual crystal deposits; use for at least 3-6 months while serum urate levels normalize
22
Q

Pharm options for acute gouty arthritis and prophylactic therapy

A
  • Acute gouty arthritis -> NSAIDs, COX 2 inhibitor, colchicine, corticosteroids
  • Prophylactic therapy -> short term = colchicine 0.6 mg BID, low dose NSAIDs; long term = allopurinol, febuxostat
23
Q

Non-pharms for gout

A
  • Avoid drugs capable of inducing hyperuricemia and gout (ex: loop and thiazide diuretics, beta blockers, ACE inhibitors salicylates < 2 g/day, pyrazinamide, nicotinic acid, omeprazole, cyclosporine and tacrolimus)
    • Can use Ca channel blockers or losartan for HTN
24
Q

NSAIDs for gout

A
  • Use recommended maximal doses at the first sign of an attack
  • Lower dose as sx resolve (4-5 days)
  • Start ASAP at max. dose then taper
  • Should also get PPI for GI protection
  • Continue until joint pain has resolved totally for at least 48 h (7-10 days)
  • No evidence that any given NSAID is superior
  • Pt should have some on hand for next acute attack (b/c having to see the Dr for every attack slows down initiation of therapy)
25
Q

NSAID doses for gout

A
  • Anti-inflammatory dose different from analgesic dose
  • Ibuprofen = 600 mg QID
  • Naproxen = 750 mg then 500 mg BID
  • Celecoxib = 400 mg q12h x 2 days then 200 mg BID
26
Q

Colchicine dosing for gout

A
  • Traditional dosing = 0.5-0.6 mg q1h or 1-1.2 mg q2h until significant improvement of pain or GI toxicity
  • Maximum total dose = 8-10 mg
  • *Should use 1.2 mg followed by 0.6 mg in 1 h!!
    • Tested 1.2 mg followed by 0.6 mg in 1 h vs. 1.2 mg followed by 0.6 mg per h x 5 h (total dose = 4.8 mg) -> conclusion = no difference in efficacy (pain reduction) but high dose caused significantly more GI effects
  • Old dosing = 1.2 mg followed by 0.6 mg/h for 5 h (don’t use this; will cause severe diarrhea, N/V)
27
Q

Colchicine drug interactions

A
  • CYP 3A4 inhibitors (diltiazem, verapamil, itraconazole, fluconazole, clarithromycin)
  • Statins and fibrates increase myalgia
28
Q

Colchicine summary

A
  • Start ASAP after the onset of a flare
  • Only use low dose, NOT traditional dosing
  • Px receiving prophylaxis therapy may receive tx dosing; wait 12 h and resume prophylaxis
  • Dosage adjustment needed w/ 3A4 inhibitors and for CrCl < 30 mL/min
29
Q

Systemic corticosteroids for gout (dose, role, and when to expect pain relief)

A
  • Prednisone 20-40 mg/day x 4 days
  • Taper over 1-2 weeks
  • Pain relief w/in 12-48 h
  • Used for refractory attacks or when other agents contraindicated
30
Q

IA corticosteroid injection for gout

A
  • Septic arthritis needs to be ruled out first
  • Single injection of methylprednisolone acetate 10-40 mg or dexamethasone 0.8-4 mg
  • Pain relief w/in 12-24 h – lasts for duration of attack
31
Q

Prophylactic therapy for gout

A
  • 7% of px won’t experience another attack for 10 years or more
  • Must consider -> severity of acute attack, response to tx, serum urate concentrations, and another change being made to decrease UA
32
Q

Short term prophylactic therapy for gout

A
  • Px w/ no tophi and normal or slightly elevated uric acid levels
  • Colchicine 0.6 mg BID
  • Low dose NSAIDs
  • D/c drugs if uric acid normal and pt is sx free for 6 months
33
Q

When to consider urate lowering therapy

A
  • Recurrent attack, arthropathy, or X-ray changes
  • Tophi
  • Gout w/ CKD
  • Recurring renal stones
  • Need for ongoing diuretic tx (after 1st gout attack)
34
Q

Goals of urate lowering therapy

A
  • Uric acid < 360 umol/L

- Can we go too low? (under investigation)

35
Q

Benefits of uric acid levels < 360 umol/L

A
  • Reduced frequency of attacks
  • Reduced tophus size
  • Deplete crystal stores in synovial fluid
  • Improved renal function w/ reduction of NSAID use
  • Slows progression of existing renal disease
36
Q

Allopurinol for gout (dose, MOA)

A
  • Blocks conversion of hypoxanthine to xanthine and xanthine to uric acid
  • Misconception about dosing (60% of px are under dosed)
  • Fear of allopurinol hypersensitivity syndrome and renal insufficiency limit its appropriate use
  • Approved from 100-800 mg
  • ~40% achieve goal urate levels w/ 300 mg/day or less
37
Q

Allopurinol hypersensitivity syndrome (AHS)

A
  • Isolated rash may occur in up to 2% of px
  • Severe cutaneous reactions, fever, eosinophilia, leukocytosis, renal involvement and hepatitis
  • Risk factors = recent onset of therapy, CKD, thiazide use
38
Q

Allopurinol summary

A
  • Initiate therapy 3+ weeks after resolution of acute attack
  • Initiate prophylaxis 2 weeks before start
  • Starting dose = 100 mg OD (50 mg OD if CrCl < 50 mL/min)
  • Titrate dose up by 100 mg q1month until target of UA < 360 umol/L
  • Can dose beyond 300 mg/day if needed
    • Don’t d/c during future flares
  • *Avoid in combo w/ azathioprine or 6-MP
39
Q

How to initiate urate lowering therapy

A
  • Initiation will increase frequency of acute attacks
  • Initiate prophylactic therapy for the first 6 months w/ colchicine 0.6 mg OD (if CrCl < 50 mL/min) or BID (if CrCl > 50 mL/min), or naproxen 250 mg BID
40
Q

Other uricosuric agents (increase excretion of uric acid in urine)

A
  • Probenicid and sulfinpyrazone -> require BID or TID dosing, many drug interactions, ineffective as CrCl decreases
  • Off label agents -> losartan, fenofibrate
41
Q

Febuxostat for gout

A
  • Potent non-purine selective inhibitor of xanthine oxidase
  • Found to be superior to allopurinol in the reduction of uric acid
    • Problem w/ study was that allopurinol dose fixed at 100-300 mg
  • Dosing -> recommended initial dose of 40 mg daily; may titrate to 80 mg daily after 2 weeks if serum uric acid > 360 umol/L
42
Q

Febuxostat or allopurinol?

A
  • Both agents effective in reduction of uric acid (if a treat-to-target approach is used)
  • Febuxostat appears to be tolerated in px w/ AHS
  • Regardless of the agent, prophylaxis w/ colchicine or NSAIDs should be used for at least 6 months after initiation of urate lowering therapy
  • Febuxostat not covered by pharmacare or private insurance
43
Q

Clinical pearls for gout

A
  • Uric acid levels can be normal during acute attack, so check levels 2-3 weeks later
  • NSAIDs -> max dose then taper and d/c 2 days after resolution of sx
  • Use only low dose colchicine for acute attacks
  • Have drug at home in preparation for next attack
  • Start urate lowering agent 2-3 weeks post-acute attack; start low and go slow
  • Don’t forget to use prophylaxis for 6 months
  • Remember to continue urate lowering therapy in acute attacks
  • Vitamin C 500-1000 mg is effective in reducing UA > 10% in 2 months
  • Increase dairy product intake
  • Spend time addressing the comorbidities of gout
44
Q

Counselling tips for acute attacks of gout

A
  • NSAIDs -> counsel pt to take w/ food to reduce stomach upset
  • Colchicine -> review dosing regimen to avoid potential toxicity
  • Steroids -> review tapering regimen and supply a calendar
  • Reassure pt that the pain should improve over the next 24-36 h
  • Adjunctive tx w/ acetaminophen +/- 8 mg codeine may be helpful initially
  • Counsel pt to reduce general alcohol consumption and to ensure they have comfortable footwear
  • Call pt in 2-3 days to check for improvement and monitor AE
45
Q

Counselling tips for prophylaxis w/ antihyperuricemic agents

A
  • Ensure pt starts w/ low doses and is clear on how to titrate
  • Ensure pt has a supply of a prophylactic NSAID or colchicine on hand to use concurrently while starting, to decrease the risk of an acute attack
  • Counsel pt to watch for potential AE and report them to pharmacist or physician
  • Inform pt that routine bloodwork will be required to monitor how well the medication is working and to avoid potential AE

Year 3 - Clinical (Winter) (30 decks)

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