Gout Flashcards

1
Q

What is gout

A

Persistent raised plasma uric acid (urate) concentrations this leads to uric acid crystal formation - painful inflammation within joints (big toe)

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2
Q

How does gout occur

A

Monosodium urate crystals (MSU) deposit in cartilage in the joint space resulting from sustained hyperuriaemia (high levels of uric acid) this leads to an inflammatory response

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3
Q

What are the symptoms of gout

A

Rapid onset (hrs/days)
Severe pain
Swelling
Redness and warmth
Tenderness in joint

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4
Q

Risk factors of gout

A

Age
Male
Obesity
Purine rich diet (red meat, seafood, alc)
Renal impairment (CKD)
Hypertension
Drugs (beta blockers, diuretics, ACEi)
Family history of gout

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5
Q

Diagnosis of gout

A

Gold standard
MSU urate crystal detection in fluid from joint
Observation, X-ray, ultrasound
Lab - serum Uric acid (SuA), CPRC and ESR

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6
Q

When to refer someone with gout to secondary care

A

URGENT ASAP - septic arthritis - generally unwell, painful hot swollen joint
- Unresponsive to uric acid lowering
- Persistent SE despite Max NSAID
- Gout complications e.g neuropathy
- Gout persists despite uric acid levels being lowered
- young onset ( below 30yrs)
- pregnancy

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7
Q

Gout acute management

A

Start ASAP for 1-2 weeks and R.I.C.E

1st line NSAIDS + PPI
2nd line colchicine
3rd line corticosteroid

If poor response can combine

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8
Q

Gout chronic management

A

DONT START during an attack (1-2 weeks after) BUT CONTINUE if already on drugs and a attack occurs

1st line allopurinol
2nd line febuxostat
3rd line benzbromarone

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9
Q

When is long term treatment (chronic) needed for gout

A

2 + attacks in year
Tophi
Young
CKD And gout
Continuing diuretics (HF) and gout
Uric acid renal stones

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10
Q

Allopurinol MOA

A

Lowers serum uric acid
Inhibits xanthine oxidase
Deposition of urate crystals in tissue (Tophi) is reversed

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11
Q

Uricosuric drugs (benzbromarone) MOA

A

Inhibits renal tubules from reabsorbing uric acid
Increase renal excretion and decrease urate levels in serum

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12
Q

Metabolism of purines to uric acid

A

Uric acid is the end product of purine nucleic acid degradation
1. Adenine and guanine are metabolised through the same pathway
2. Deamination occurs of adenine
3. Ribose-5-P removal
4. BOTH are converted to xanthine
5. Converted to uric acid
6. Uric acid is renally excreted

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13
Q

Colchicine SERIOUS SE

A

STOP severe nausea and vomiting

SAME day assessment If take too much (even if no SE)

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14
Q

Colchicine Ci and cautions

A

CI HF
Caution/ low dose - fluoxetine, erythromycin
Renal impairment and statin and elderly

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15
Q

Allopurinol SERIOUS SE

A

STOP if rash but if mild and resolves can continue if rash again DISCONTINUE

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16
Q

Allopurinol CI and cautions

A

AVOID azathioprine (inhibits metabolism of azathioprine - accumulation of toxic metabolites)

Dose adjustments in renal impairment

Don’t start during an attack (1-2 weeks after) but if already taking continue

17
Q

Febuxostat SERIOUS SE

A

STOP if hypersensitivity
DISCONTINUE do not restart

18
Q

Febuxostat CI and cautions

A

AVOID azathioprine
CI - liver impairment, HF, thyroid