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M202 > W32 Gout (JD) > Flashcards

W32 Gout (JD) Flashcards

1
Q

What is gout?
2 most common crystals

A

Insoluble crystals are deposited in areas of the body leading to symptoms

– Monosodium urate = “gout”
– Calcium pyrophosphate =“pseudogout”

  • In typical gout – crystals form in joint leading to arthritic pain
    Gout – a “crystal deposition disease”
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1
Q

For info ([2nd-century Greek physician Aretaeus, describing the pain of gout]

A

No other pain is more severe than this, not iron screws, nor cords, not the wound of a dagger, nor burning fire.

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2
Q

Gout – a “crystal deposition disease”
- Features of gout

A
  • Disease spectrum of hyperuricemia
    – Uric acid ≥ 360 μl/L
  • High plasma urate = most important determinant for gout
    – risk increases exponentially
  • may be asymptomatic
    – (generally, do not treat)
  • Deposits of urate crystals in joints
  • Deposits of urate crystals in connective tissues (tophi),
  • Deposits of uric acid in kidney -nephrolithiasis (kidney stones)
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3
Q

Gout
What does Deposition of urate crystals in synovial fluid lead to? (3)

A
  • Macrophages phagocytose Mono Sodium Urate (MSU) crystals → triggers cell lysis →discharge of proteolytic enzymes
  • This results in an inflammatory reaction
    with intense joint pain, erythema, warmth and swelling
  • If untreated, can result in extensive joint destruction and tophi formation (nodular accretion of MSU)
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4
Q

Epidemiology of gout:
* Serum urate concentration (and risk of gout) increases with…?

A
  • Age
  • Male gender (~ 10x more than women)
  • High blood pressure
  • Renal impairment
  • Body weight
  • High alcohol and soft drink intake, meat, seafood
  • Metabolic X syndrome (insulin resistance – risk of type 2 diabetes/cardiovascular events – high BMI values)
  • Certain medicines – (e.g., diuretics, low-dose aspirin)
  • Familial tendency
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5
Q

Etiology of gout:
Overproduction of uric acid:

A
  • Cytotoxic drugs, radiotherapy (increased
    cell destruction)
  • Obesity, excessive consumption of
    alcohol, or purines (meat)
  • Inherited enzyme defect
  • High cell turnover (neoplastic diseases,
    psoriasis
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6
Q

Etiology of gout
Under-excretion of uric acid

A
  • Diuretics (especially thiazides), low dose
    aspirin, ciclosporin
  • Renal impairment
  • Heart failure
  • Metabolic causes such as ketosis (DM), starvation
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7
Q

Pathophysiology of gout?

A

Purines, from which uric acid is produced,
originate from three sources:
- Dietary purines
- Conversion of tissue nucleic acid to purine
nucleotides
- De novo synthesis of purine base

  • These purine precursors are metabolised by
    the liver to uric acid – 2/3 cleared by the
    kidneys and 1/3 by the GIT
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8
Q

What are 4 foods to avoid eating with gout?

A
  1. Alcohol
  2. Soft drinks
  3. Seafood
  4. Liver
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9
Q

Diagnosis of gout?
What steps are involved in diagnosis?

A
  • History
    -Dietary habit, comorbidities, family Hx, Drug Hx
  • Signs and symptoms
    -Rapid onset (often overnight) of severe pain together with redness and swelling in one or both metatarsophalangeal (MTP) joints.
  • Serum urate level
  • A serum urate level of ≥ 360 micromol/L (6mg/dL) confirm the diagnosis
  • Crystals of urate in aspirate of synovial fluid (rarely performed)
  • To identify crystals and hence type of gout
  • Response to treatment
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10
Q

Differential diagnosis of gout:

A
  • Bursitis, tenosynovitis, cellulitis
  • Haemochromatosis
  • Non-urate crystal-induced arthropathy, such as pseudogout
    * Osteoarthritis
  • Psoriatic arthritis
  • Reactive arthritis
  • Rheumatoid arthritis
  • Septic arthritis
  • Trauma
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11
Q

What are the phases of gout? (2)

A

Acute
Chronic

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12
Q

Clinical presentation of acute gout?

A
  • Men more than women, often 40-60 years old
  • Rapid onset of intense pain, swelling, redness and inflammation in affected joint
    -Maximum severity reached within 12-24 hours
  • Acute attacks can be very severe - may mimic septic arthritis, with fever, malaise, leucocytosis and raised inflammatory markers
  • Often begins at night, waking the sufferer from sleep (likely due to colder temperatures)
  • Untreated attacks may last 3-14 days before spontaneous recovery
  • Most typically affects one joint initially
    -Most often occurs in the big toe (podagra)
    -Other sites: ankle, heel, knee, wrist, finger, elbow
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13
Q

Chronic (tophaceous) gout
Clinical presentation?

A
  • Eventually recurrent attacks may fail to
    resolve completely → crippling destructive arthritis.
  • Tophi – (firm, white nodules under translucent skin) after 10 -20 years.
    -Common sites of tophaceous gout: elbows, hands, feet
    -Less common sites: helix of the ear, Achilles tendon and knee joints
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14
Q

Treatment goals and desired outcomes in..

A

Acute gout:
* Terminate attack and provide symptom relief
Chronic gout:
* Prevent acute attacks
* Prevent joint destruction and disability
* Resolve tophi
* Prevent nephrolithiasis and renal disease
Asymptomatic hyperuricaemia:
* Treatment is not usually indicated
* Address lifestyle factors

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15
Q

Management of acute gout:
What medications are used first-line? (3)

A
  • NSAIDs – 1st Line
  • Colchicine – 1st Line
  • Corticosteroids – 1st Line
16
Q

NSAIDs- acute gout

A
  • Treatment of choice when not contraindicated
  • Does not modify plasma urate concentrations
  • Probably all equally effective
    -Naproxen is most commonly used
    -short acting, easily titrated
  • Start with high dose until symptoms start to resolve (usually 3-5 days) then
    reduce dose until signs of joint inflammation resolve (then cease)
  • Consider PPU with NSAIDs
17
Q

Corticosteroids- acute gout

A
  • Another option if NSAID is contraindicated
  • A short course of oral corticosteroid — for example prednisolone 30-35 mg once a day for 3-5 days.
    -Note: this is an off-label use of oral corticosteroids.
  • Corticosteroids can be given as an intra-articular injection – where 1 or 2 joints are affected
18
Q

Colchicine- MoA

A
  • Colchicine – an inhibitor of cellular microtubule function
  • Inhibits neutrophil migration, chemotaxis, adhesion and phagocytosis in the inflamed area; reduces inflammatory reaction
  • No effect on uric acid production or excretion
19
Q

Colchicine – Toxicity
For info- (extract from an article)

A

● “near universally fatal consequence of a significant overdose”
● “cases series of 9 patients…. with a colchicine overdose”
● “significant number were accidental”
● “all cases, apart from one, resulted in death”

20
Q

Acute gout – Colchicine
Dose?

A

Adult
* 500 micrograms orally 2–4 times a day until symptoms relieved
* Maximum 6 mg per course, do not repeat course within 3 days

21
Q

Colchicine – other information
common se?

A
  • Do not repeat the course within 3 days
  • Takes 24 to 48 hours to relieve symptoms
  • Signs of toxicity often occur within 24 hours of starting therapy, usually before pain subsides
  • Common SE: nausea, vomiting, diarrhoea
  • Severe SE: multi-organ failure, neuropathies, cardiovascular failure, low blood counts, convulsions, coma and death
  • Drug interactions – Colchicine is a substrate of both cytochrome P450 3A4 and P glycoprotein
22
Q

Management of chronic gout
Prophylactic treatment: Urate lowering therapy ( ULT)– two classes?

A
  • Xanthine oxidase inhibitor – Decreases production of urate
  • Such as allopurinol & febuxostat (1st line)
  • Uricosuric agent – Increases renal excretion of uric acid
  • Such as sulfinpyrazone or benzbromarone (specialist use – 2nd line)
23
Q

Urate lowering therapy (ULT)
Indicated in? (4)

A
  • Tophaceous gout
  • Non-tophaceous gout if acute attacks are frequent
  • CKD
  • Chronic gouty arthritis
  • ULT is a lifelong treatment – even if serum urate level is achieved .
  • ULT to be started at least 2- 4 weeks after a flare
  • Titrate the dose until target urate level achieved
24
Q

Serum urate monitoring:

A
  • Use monthly urate level to guide dose titration of ULT
  • Once target achieved with ULT – consider annual monitoring of serum urate

Targets:
Chronic gout = < 360 μl/L
Tophaceous gout or those with frequent
flare despite serum urate level < 360 μ/L
= < 300 μ/L

25
Q

Urate lowering therapy:
First line?
Give with what other medication?

A
  • Allopurinol
  • Febuxosta

Give with colchicine, NSAID or prednisolone on commencement to prevent exacerbation of gout (for ~ 6 months)

26
Q

Allopurinol
What drug class?
When should it not be started?
- exception?

A
  • Xanthine oxidase inhibitor that decreases production of urate
  • Allopurinol should not be started during acute gout, due to the potential for worsening the arthritis when there are sudden changes to urate levels
  • However, if the patient is taking allopurinol (already), it should always be continued during an acute attack.
27
Q

Allopurinol
SE?
Monitoring?

A
  • Common SE: Rash
  • Severe SE: Severe cutaneous adverse reactions, hypersensitivity, hepatic disorder
  • Monitor LFT
    -Dose adjustment in hepatic impairment
  • Monitor RFT
    -Renal impairment → increased risk of drug accumulation
    → increased risk of hypersensitivity
    -Manufacture recommends dose adjustment
28
Q

Febuxostat:
When to use?

A
  • Novel, orally administered, non–purine analogue inhibitor of xanthine oxidase
  • Biochemically unrelated to allopurinol therefore may be an alternative if intolerant to allopurinol
  • More effective urate-lowering than allopurinol
    300mg BUT no fewer gout attacks (CONFIRMS
    trial)
29
Q

Febuxostat- more info
Main SE?

A
  • Mainly eliminated by glucuronidation in the liver
    -Manufacturer advises max. 80 mg daily in mild impairment
  • No dose adjustments are recommended in patients with mild to moderate renal impairment →no data re severe impairment
  • Main side effects – liver function abnormalities, diarrhoea, headache, nausea and rash.
  • Sever SE – Serious hypersensitivity reactions, Increase risk of CV death in patient with Hx of major CVD (Clinical trial)
    -MHRA/CHM Advice
30
Q

Nonpharmacologic advice in chronic gout? (4)

A
  • Diet – healthy, well-balanced diet
  • Weight management – obesity can exacerbate flare
  • Reduce alcohol intake – excess alcohol can exacerbate gout
  • Advice to treat attack asap and that prophylactic treatment should not be discontinued
31
Q

Nonpharmacologic advice - NHS

A
  • Get to a healthy weight but avoid crash diets- try the NHS weight loss plan
  • Eat a healthy, balanced diet- your gp may give you a list of foods to include or limit
  • Have some alcohol free days each week
  • Drink plenty of fluids to avoid getting dehydrated
  • Exercise regularly- but avoid intense exercise or putting lots of pressure on joints
  • Stop smoking
  • Ask a GP about vitamin C supplements

Dont:
- have lots of sugary drinks and snacks
- eat a lot of fatty foods
- drink more than 14 units of alcohol a week, and spread your drinking over 3 or more days if you drink as much as 14 units

32
Q

When is a referral needed for gout?
(to a rheumatology service) (4)

A
  • The diagnosis of gout is uncertain
  • Treatment is contraindicated, not tolerated or ineffective
  • Patients with CKD stages 3b to 5 (K&L ISU)
  • Those who have had an organ transplant
33
Q

Which of the following drugs is the MOST appropriate option for patient with chronic gout and myocardial infarction?
A. NSAIDs
B. Febuxostat
C. Allopurinol
D. Sulfinpyrazone

A

= C
- clinical guidelines for gout recommend allopurinol as first-line treatment for patients with gout and major cardiovascular disease

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