Gout Flashcards

(47 cards)

1
Q

What is the underlying pathophysiology of gout?

A

Deposition of monosodium crystals in:
- Joints
- Soft tissue (cartilage, tendons, bursae)
-Renal tissues (glomeruli, interstitium, tubules)

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2
Q

What clinical conditions can result from MSU crystal deposition?

A
  • Gouty arthritis
  • Tophi
  • Urate nephropathy
  • Uric acid nephrolithiasis
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3
Q

What is the most common cause of inflammatory arthritis in men over 40 years?

A

Gouty arthritis

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4
Q

What is the typical age of onset of gout in men & women?

A

Men: 4th decade

Women: 6th decade

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5
Q

When is gout considered unusual & suggestive of an underlying disorder?

A

Men < 30 years
Women < 50 years

Suggests possible inherited enzyme abnormality

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6
Q

What is the current epidemiologic trend of gout?

A

Increasing incidence & prevalence

Reflects growth of at risk populations

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7
Q

What metabolic condition is gout strongly associated with?

A

Metabolic syndrome

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8
Q

How does reduction of serum uric acid levels affect renal function in patients with gout?

A

Greater reduction in serum uric acid
- Greater preservation in renal function

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9
Q

What cardiovascular risk is associated with gout in middle aged men?

A

Increased CV mortality

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10
Q

What are the Goals of Therapy?

A
  • Terminate the acute attack of arthritis
  • Prevent recurrence
  • Prevent or reverse complications
  • Treat associated disorders
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11
Q

What is asymptomatic hyperuricemia?

A

Elevated serum urate with no clinical manifestations

Thresholds:
>360 μmol/L in females
>420 μmol/L in males

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12
Q

Is asymptomatic hyperuricemia an indication for urate-lowering therapy?

A

No - ULT is not indicated

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13
Q

What is the typical clinical course of asymptomatic hyperuricemia?

A

Most patients remain asymptomatic for life

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14
Q

In which patients should causes of uric acid overproduction be assessed?

A

Onset before age 25

History of urolithiasis

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15
Q

What drugs are associated with Hyperuricemia & Gout?

A

Alcohol

Cyclosporine

Cytotoxic chemotherapy

Diuretics (only thiazide & loop)

Ethambutol

Interferon + ribavirin

Levodopa

Nicotinic acid (niacin)

Pyrazinamide

Salicylates, low dose

Tacrolimius

Teriparatide

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16
Q

What conditions are associated with Hyperuricemia & Gout?

A

Alcohol intake (excessive consumption)

Atherosclerosis

Chronic kidney, glomerular, interstitial renal disease

Diabetes

Dietary factors (purine, high-fructose corn syrup)

Hyperlipidemia

HTN

Ischemic heart disease

Lead intoxication

Metabolic syndrome

Myeloproliferative disorders and some cancers

Obesity

Urolithiasis history

Rarely genetic or acquired causes of uric acid overproduction

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17
Q

What are common precipitants of an acute gout attack?

A

Acute illness

Surgery

Trauma

Alcohol

High purine diet

Medications

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18
Q

How does an acute gout flare typically present?

A

Abrupt onset

Severe, excruciating pain

Often occurs at night or early morning

Unable to tolerate light pressure

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19
Q

What is the typical duration of an acute gout attack?

A

Resolves spontaneously in 3-10 days

May last longer in patients with > 10 years of gout

20
Q

What chronic finding may be present on physical exam in gout?

A

Tophi (subcutaneous urate deposits)

21
Q

How should serum urate levels be interpreted during an acute gout flare?

A

May be normal during an acute attack

Normal urate does NOT exclude gout

22
Q

What is the gold standard test for diagnosing acute gout?

A

Synovial fluid analysis for identification of monosodium urate crystals

23
Q

What imaging modalities can support the diagnosis of gout? Why?

A

Ultrasound
Dual energy CT or x-ray

For evidence of urate deposition or evidence of joint damage

24
Q

Which joints are most commonly affected in gout?

A

Lower limb joints are most commonly affected

25
How does joint involvement in gout differ between men & women?
Upper limb involvement is more frequent in women than men
26
What is the typical joint pattern of the first gout attack?
Monoarticular in ~85% of first attacks Polyarticular presentation more common in older patients
27
What is a podagra? How common is it?
Inflammation of the first metatarsophalangeal (MTP) joint Involved in >50% of first attacks Develops in >90% of patients over time
28
Which other joints are commonly affected in gout (in decreasing order)?
Insteps Ankles Heels Knees Wrists Interphalangeal joints Elbows
29
What triad supports a presumptive diagnosis of gout?
Acute monoarthritis Hyperuricemia Dramatic response to colchine
30
What is required for a definitive diagnosis of gout?
Identification of intracellular monosodium urate crystals in synovial fluid
31
What non-pharmacologic therapy can be used as an adjunct in acute gouty arthritis?
Topical ice application - Helps reduce inflammation - Used in addition to one or more pharmacologic treatments
32
When should treatment of an acute gout flare be initiated?
ASAP after symptom onset Ideally within the first 24 hours
33
What are first line treatment options for an acute gout flare?
- Colchicine - NSAIDs - Corticosteroids
34
What is a key treatment principle in managing acute gout?
Early treatment leads to better outcomes Do not delay therapy while awaiting confirmatory tests
35
What is the recommended colchine dosing for an acute gout flare?
1.2 mg initially then 0.6 mg 1 hr later (for a total of 1.8 mg)
36
When & how is colchicine used for gout prophylaxis after an acute flare?
Start 12 hours after last acute treatment dose 0.6 mg once to twice daily
37
How are NSAIDs used in acute gout flares? Why?
Initiated at high doses then quickly reduced once improvement occurs Effective in reducing pain & swelling
38
Who is at higher risk of NSAID adverse effects in gout treatment?
Older patients with renal dysfunction
39
How do COX-2 inhibitors compare to nonselective NSAIDs in gout?
Equally effective for pain relief Fewer adverse effects Better tolerability
40
What NSAID strategy is preferred in patients at risk for ulcer complications*?
Celecoxib + PPI Alternatives - Celecoxib alone - Nonselective NSAID + PPI *Age >65 *Previous GI bleed *Comorbid medical conditions *Low dose ASA *Anti-coagulant use
41
What CV risks are associated with NSAIDs?
- Heart attack - Stroke - HF Risk is increased with higher doses & long term use Avoid in patients with heart disease or at increased risk of cardiovascular events
42
What is the role of corticosteroids in acute gout flares?
- Third option for gout flare therapy - As effective as NSAIDs in reducing pain (at rest or with activity)
43
How are oral corticosteroids used in acute gout?
Short term course of prednisone e.g., 0.5 mg/kg/day <21 days no taper needed
44
When are intra-articular, IM, or IV corticosteroid preferred in gout?
When oral therapy not tolerated
45
When is intra-articular corticosteroid therapy NOT ideal in gout?
Polyarticular involvement
46
When & how is combination therapy used in acute gout?
Indications - Symptoms are severe - Attack is polyarticular - Large joints involved - Poor response to monotherapy Options - Colchicine + NSAID - Colchicine + Corticosteroid - Intra-articular steroid + NSAID / oral steroid / colchicine
47
What are some therapeutic tips for an acute gout attack?
Earlier therapy is started -> the more quickly the attack will be resolved Do not stop or alter the dose of urate-lowering drugs during an acute attack, because symptoms may be exacerbated or prolonged