Acute Management of Gout Flashcards

1
Q

What causes gout?

A

Caused by a build up and deposition of sharp needle-like monosodium urate crystals in areas of slow blood flow like the joints and renal tubules

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2
Q

What do purines and pyrimidines both contain?

A

Nitrogen atoms

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3
Q

What are purines and pyrimidines key components of?

A

Nucleic acids (found in DNA, RNA)

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4
Q

What is the relationship between purines, pyrimidines and gout?

A

When cells and the NA’s within those cells breakdown, the purines are also broken down into uric acid, this uric acid can be filtered out of the blood and excreted in the urine, uric acid has limited solubility in body fluids and can manifest as hyperuricaema when the rate as which it is made exceeds solubility, uric acid can lose an ion (at pH 7.4) to become urate, combined with sodium this becomes monosodium urate, crystals can form due to increased ingestion of purines or internal sources

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5
Q

What foods are high in purines?

A

Liver and kidneys, game, oily fish, seafood, meat and yeast extracts (marmite, gravy), soft drinks, alcohol (especially beer, stout, port)

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6
Q

What foods are low in purines?

A

Dairy, eggs, breads and cereal, pasta and noodles, fruit and vegetables

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7
Q

What foods can lower serum uric acid levels/help its excretion?

A

Dairy products can lower serum uric acid levels

Cherries are high in vitamin C and also help to increase uric acid excretion

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8
Q

What are some of the risk factors for developing gout?

A

Increased purine intake, overproduction of urine acid, loop and thiazide diuretics, taking medications that can raise uric acid levels (aspirin, ciclosporin), genetic predisposition, obesity, hypertension, dyslipidaemia, alcohol intake, male gender

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9
Q

Why are loop and thiazide diuretics associated with the development of gout?

A

Kidney excretes around 2/3 of the uric acid produced by the body (remainder is excreted via the biliary tract), loop and thiazide diuretics cause volume depletion and reduce tubular renal secretion of uric acid

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10
Q

What are some of the key symptoms of gout?

A

Usually affects the first metatarsal joint of the big toe (known as podagra), extremely painful and will wake patient up with a feeling their toe is ‘on fire’, other joints can be affected (elbows, knees etc.)

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11
Q

When is the pain of gout worst?

A

In the hours following the attack and then lessens with time, but can last from days to weeks

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12
Q

What causes the symptoms of gout?

A

The area becomes inflamed due to migration of WBC’s (leukocytes) to eliminate uric acid and release cytokines

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13
Q

What can happen if a patient has repeat attacks of gout?

A

Can develop chronic gout, a type of arthritis with joint tissue destruction and deformity
Chronic gout can also lead to a permanent build up of urate crystals tophi which form along the bones underneath the skin

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14
Q

What are patients with chronic gout at an increased risk of developing?

A

Kidney stones (made of urate crystals) and urate nephropathy

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15
Q

What are the 2 main aims of management of gout?

A

To relieve pain and swelling so 1st line treatment is NSAID’s, where NSAID’s are not suitable colchicine can be used
To maintain serum uric acid levels below saturation point, if this is done, crystal deposits dissolve

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16
Q

When should treatment for an attack be started?

A

NSAID’s should be started immediately at high doses which are then reduced 24 hours after complete resolution of the attack
Colchicine should also be started immediately (takes around 6 hours to action vs. 2 hours in NSAID’s)

17
Q

Should treatment for an attack of gout be given continually?

A

NSAID’s should not be used continually

18
Q

What is the mode of action of Colchicine?

A

Arrests the assembly of microtubules in neutrophils and inhibits various cell functions

19
Q

What is given as last line treatment in gout?

A

Corticosteroids can be given where both NSAID’s and colchicine are C/I, can be given orally, IM or IA

20
Q

What are some of the key counselling points for a patient taking Colchicine?

A

Rest the joint and use an ice pack to reduce inflammation
Be careful when using other medications such as PI’s, macrolides and ciclosporin
Ensure the patient doesn’t have severe renal impairment or chronic heart failure
Monitor vitamin B12 levels as absorption may be impaired

21
Q

When is uric acid lowering therapy required?

A

If a patient has 1 or more acute attacks within 12 months of an initial attack
In some patient groups, it is appropriate to start prophylaxis after the first attack, those with visible tophi, uric acid stones and those who need to continue on diuretics

22
Q

What drugs are used in uric acid lowering therapy and how do they work?

A

Allopurinol - inhibits the action of the enzyme xanthine oxidase and in turn reduces the production of uric acid
Febuxostat - xanthine oxidase inhibitor, more selective and potent
Uricosurics - increase uric acid excretion

23
Q

What lifestyle advice can be given to patients to prevent gout reoccurance?

A

Moderate physical exercise (not intense as this can raise uric acid levels due to increased cell turnover)
Lose weight
Ensure purine intake <200mg/day
Alcohol consumption <14 units/week and 3 alcohol free days/week