Gout Flashcards
What physiological phenomenon causes gout
Gout is caused by the build up and deposition of sharp needle-like crystals of monosodium urate in areas of slow blood flow like the joints and renal tubules
What physiological phenomenon causes gout
Gout is caused by the build up and deposition of sharp needle-like crystals of monosodium urate in areas of slow blood flow like the joints and renal tubules
Where does the uric acid come from
Purines and pyrimidines are both contain nitrogen atoms
Purines are key components of nucleic acids (found in DNA, RNA). When cells and the nucleic acids within those cells breakdown throughout the body, the purines are broken down into uric acid. Uric acid can be filtered out of the blood and then excreted into the urine
Why can uric acid cause problems when its usualy dealt with automatically by the body
Uric acid has limited solubility in body fluids, it will manifest as hyperuricaema when the rate at which it is made exceeds solubility. Uric acid can lose an ion (at pH 7.4) to become urate, and this can combine with the sodium ion to become monosodium urate (i.e. the sharp needle link crystals).
Which foods contain high, moderate and low amounts of purines
High - Offal, Game, Oily fish, Seafood, Meat and yeast extracts
Medium - Meat/poultry,
Mushrooms and mycoprotein,
Dried peas, beans and legumes,
Some vegetables – asparagus, cauliflower, spinach, Wholegrains
Low - Dairy, Eggs, Bread and cereals (except wholegrain), Pasta and noodles, Fruit and vegetables
What are the risk factors for developing gout
Increased purine intake Overproduction of uric acid Taking loop and thiazide diuretics Some medicines that can raise uric acid levels Genetic predisposition Obesity Hypertension Dyslipidaemia Alcohol intake (leads to dehydration and subsequent causes decreased clearance of uric acid) Male gender
Why are loop and thiazide diuretics associated with the development of gout
Loop and thiazide diuretics cause volume depletion and reduced tubular renal secretion of uric acid and are commonly associated with the development of gout
Which medicines are known to raise uric acid levels
Aspirin
Ciclosporin
Cytotoxic medicines
Diuretics (loop and thiazide)
Ethambutol
Levodopa
Pyrazinamide
Ribavarin and interferon
TeriparatideWhat are the key symptoms of gout and which presents first
Crystals build up underneath the skins
Yellow or white bumps (tophi)
can damage joints
Gout usually affects the first metatarsal joint of the big toe – this is known as podagra.
Where does the uric acid come from
Purines and pyrimidines are both contain nitrogen atoms
Purines are key components of nucleic acids (found in DNA, RNA). When cells and the nucleic acids within those cells breakdown throughout the body, the purines are broken down into uric acid. Uric acid can be filtered out of the blood and then excreted into the urine
Why can uric acid cause problems when its usualy dealt with automatically by the body
Uric acid has limited solubility in body fluids, it will manifest as hyperuricaema when the rate at which it is made exceeds solubility. Uric acid can lose an ion (at pH 7.4) to become urate, and this can combine with the sodium ion to become monosodium urate (i.e. the sharp needle link crystals).
Which foods contain high, moderate and low amounts of purines
High - Offal, Game, Oily fish, Seafood, Meat and yeast extracts
Medium - Meat/poultry,
Mushrooms and mycoprotein,
Dried peas, beans and legumes,
Some vegetables – asparagus, cauliflower, spinach, Wholegrains
Low - Dairy, Eggs, Bread and cereals (except wholegrain), Pasta and noodles, Fruit and vegetables
What are the risk factors for developing gout
Increased purine intake Overproduction of uric acid Taking loop and thiazide diuretics Some medicines that can raise uric acid levels Genetic predisposition Obesity Hypertension Dyslipidaemia Alcohol intake (leads to dehydration and subsequent causes decreased clearance of uric acid) Male gender
Why are loop and thiazide diuretics associated with the development of gout
Loop and thiazide diuretics cause volume depletion and reduced tubular renal secretion of uric acid and are commonly associated with the development of gout
Which medicines are known to raise uric acid levels
Aspirin
Ciclosporin
Cytotoxic medicines
Diuretics (loop and thiazide)
Ethambutol
Levodopa
Pyrazinamide
Ribavarin and interferon
TeriparatideWhat are the key symptoms of gout and which presents first
Crystals build up underneath the skins
Yellow or white bumps (tophi)
can damage joints
Gout usually affects the first metatarsal joint of the big toe – this is known as podagra.
What happens when gout attacks occur repeatedly
Repeat gout attacks can develop into chronic gout (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. Patients with chronic gout are also at increased risk of developing kidney stones (made of urate crystals) and urate nephropathy,
WHat are the aims of treatment for gout and how do we
The aim of the treatment is relieve pain (and swelling) rapidly.
1st line treatment is NSAIDS and if they are not suitable then colchicine can be used. It is thought the mode of action relates to the migration of white blood cells – arresting the assembly of microtubules in neutrophils and inhibiting various cell functions. Colchicine takes around 6 hours to take actions versus 2 hours for an NSAID
If NSAIDS or colchicine contraindicated or ineffective = Corticosteroids
What are the side effects and councelling points for colchicine
Common side effects include abdominal cramps, nausea and vomiting. Rarely, bone marrow suppression, neuropathy and myopathy can also occur.
What is the aim of prophylaxis of gout
Aim of prophylaxis is to;
Maintain serum uric acid levels below the saturation point of monosodium urate; if serum urate is maintained below this level, crystal deposits dissolve
How do we treat gout for prophylaxis pharmocologically
If a patient has 1 or more acute attaches within 12 months of an initial attack, uric acid lowering therapy will be required to prevent further flare-ups. In some patient groups it may be appropriate to start prophylaxis after the first attack – those with visible tophi, those with uric acid stones and those who need to continue on diuretics. The drugs we use are:
Allopurinol
Febuxostat
Uricosurics
Start medication 2-3 weeks after an acute attack has completely resolved.
How does allopurinol work to treat gout
It inhibits the action of the enzyme xanthine oxidase, thus reducing the production of uric acid.
How does Febuxostat work to treat gout
Febuxostat is a more selective and potent inhibitor of xanthine oxidase than allopurinol, and has no effect on other enzymes involved in purine or pyrimidine metabolism.
How do Uricosurics work to treat gout
Uricosuric medicines that increase excretion of uric acid, have traditionally been used to manage gout but are less relevant clinically now
How can a patient modify their lifestyle to help prevent gout attacks
Engaging with moderate physical exercise (not intense as this can raise uric acid levels due to increased cell turnover)
Lose weight gradually if overweight
Ensure purine intake is no more than 200mg/day
Men should restrict alcohol consumption to less than 14 units per week (updated recommended limit)
Men and women should have 3-alcohol free days/week
