Disease caused due to deposition of uric acid

1. BY CHARLEE S.
GOUT

3. INTRODUCTION & HISTORY
• The term Gout is derived from the Latin Gutta, which
means a drop. In the 13th century, it was thought that gout
resulted from a drop of evil humor affecting a vulnerable
joint.
• It is a disease in which tissue deposition of monosodium
urate (MSU) crystals occurs as a result of hyperuricemia
(MSU supersaturation of extracellular fluids), resulting in
one or more of the following manifestions: gouty arthritis
(pain and swelling in the joints), tophi (aggregated deposits
of MSU occurring in the joints and soft tissue (muscles),
gouty nephropathy (impairment of kidney function due to
gout), uric acid nephrolithiasis (uric acid deposition in the
kidney).

5. • Throughout history, gout has been associated with rich
foods and excessive alcohol consumption.
• Because it is clearly associated with a lifestyle that, at
least in the past, could only be afforded by the affluent,
gout has been referred to as the ‘disease of kings’.
• Although there is evidence that colchicine, an alkaloid
derived from the autumn crocus (Colchicum autumnale),
was used as a powerful purgative in ancient Greece
more than 2000 years ago, its first use as a selective
and specific treatment for gout is attributed to the
Byzantine Christian physician Alexander of Tralles in the
sixth century AD.

6. CAUSES
• Gout is caused by the buildup of too much uric acid in
the body.
• Uric acid comes from the breakdown of substances
called purines.
• Purines are found in all of your body’s tissues.
• They are also in many foods, such as liver, dried beans
and peas, and anchovies.

7. URIC ACID CRYSTALS

8. • Normally, uric acid dissolves in the blood.
• It passes through the kidneys and out of the body in
urine.
• But uric acid can build up in the blood when:-
• The body increases the amount of uric acid it makes.
• The kidneys do not get rid of enough uric acid.
• A person eats too many foods high in purines.

9. • Hyperuricemia is increased levels of uric acid in the
blood & is defined as a serum uric acid concentration.
• Diet, genetic predisposition, or underexcretion of urate.
• Most people with hyperuricemia do not develop gout.
But if excess uric acid crystals form in the body, gout
can develop.

12. You are more likely to have gout if you:
• Have family members with the disease
• Are a man
• Are overweight
• Drink too much alcohol
• Eat too many foods rich in purines
• Have an enzyme defect that makes it hard for the body to break down purines
• Are exposed to lead in the environment
• Have had an organ transplant
• Use some medicines such as Diuretics, Aspirin, Cyclosporine, or Levodopa
• Take the vitamin Niacin.
• Female patients develop gout at an older age (typically after menopause).

13. SYMPTOMS
• For many people, the first attack of gout occurs in the
big toe.
• Often, the attack wakes a person from sleep.
• The toe is very sore, red, warm, and swollen.

15. Gout can cause:-
• Pain
• Swelling
• Redness
• Heat
• Stiffness in joints.

17. • A gout attack can be brought on by stressful events,
alcohol or drugs, or another illness.
• Early attacks usually get better within 3 to 10 days,
even without treatment.
• The next attack may not occur for months or even
years.

18. ACUTE GOUT
• Acute gouty arthritis – the first episode.
• Usually preceded by Hyperuricemia for years.
• It is a medical disorder that deserves specific
studies and its own labeled indication
OR
• a model of acute pain.

21. CHRONIC GOUT
Those with chronic arthritis symptoms include:-
• joint damage and
• loss of motion in the joints.
• joint pain and other symptoms most of the time.
• Tophi below the skin around joints or in other places.
Tophi usually develop only after a patient has had the
disease for many years.

23. DIAGNOSTIC TESTS
• Synovial fluid analysis (shows uric acid crystals)
• Uric acid – blood
• BUN (Blood Urea Nitrogen)
• Joint X-Rays(may be normal)
• Synovial biopsy
• Uric acid – urine
• Creatnine level

26. TREATMENT

27. • Doctors use medicines to treat an acute attack of gout,
including:
• Non-steroidal anti-inflammatory drugs (NSAIDs)
• Corticosteroids, such as prednisone
• Colchicine, which works best when taken within the
first 12 hours of an acute attack
• Febuxostat
• Uricosuric drugs

28. NON-STEROIDAL ANTI-INFLAMMATORY
DRUGS (NSAIDS)
• NSAIDs such as Diclofenac, Naproxen or Ibuprofen relieve pain
and help to reduce the redness and swelling.
• They are usually very effective and do not contain steroids.
• They can, however, sometimes give rise to indigestion or an
upset stomach.
• Rarely NSAIDs can cause stomach ulcers, bleeding and rashes.
• They can also aggravate asthma, heart and kidney failure and
raise blood pressure.
• However, these more serious side effects are very uncommon
with short term use.
• NSAIDs should be used at the lowest possible dose for as short
a duration as possible.

29. • Newer NSAIDs called COX-2 selective inhibitors (‘coxibs’)
are less likely to cause stomach upsets or gastric bleeding,
and are
• therefore sometimes recommended for patients who are at
higher risk of suffering an ulcer or bleed.
• Coxibs should be avoided in people with a history of heart
problems such as heart attack, heart failure, angina or
bypass surgery and all NSAIDs should be used with great
care in patients with hypertension, heart and kidney
disease.

30. CORTICOSTEROIDS
• Corticosteroids such as Prednisone.
• Intra-articular injection, dose dependent on the
joint.Have to make sure you have the diagnosis before
injecting.
• Side effects with a short course are usually limited to mild
insomnia or flushing.
• Long term treatment with corticosteroids is best avoided as
it can result in weight gain, fluid retention, high blood
pressure and diabetes, as well as osteoporosis and wasting
of the skin and muscles.

31. URICOSURIC DRUGS
• Probenecid and Sulfinpyrazone.
• Probenecid is well tolerated.
• Can’t use if kidney stones, renal insufficiency.
• Some drug interactions.
• Need to produce at least 1500 ml urine per day.
• Target is < 6 uric acid level.
• Need a 24 hour urine for uric acid to demonstrate not an
overproducer.

32. • Sulfinpyrazone is a metabolite of phenylbutazone.

33. ALLOPURINOL
• Inhibits synthesis of uric acid by inhibiting xanthine oxidase enzyme.
• It is usually started in a small dose of 100mg daily and this is then
gradually
• increased as instructed by your doctor.
• However, people with poorly functioning kidneys, whatever the cause,
should receive a reduced dose.
• Skin rashes are a troublesome complication in less than 5% of gout
patients.
• Rarely, however, these can be serious and severe, so it is advisable
• to consult your doctor if a rash develops.

35. FEBUXOSTAT
• Febuxostat is a newer drug used for the treatment of
patients with gout who are unable to tolerate
allopurinol, or who have failed to respond adequately to
optimal doses.
• It acts in a similar way to allopurinol, but may be more
powerful at reducing uric acid levels, and may be more
suitable for those with poor renal (kidney) function.
• However, it is unsuitable for patients with ischaemic
heart disease such as angina.

36. PREVENTION
To help prevent the gout:-
 Follow a healthy diet.
 Avoid alcohol use, especially beer drinking.
 Lose weight if you are obese.
 Avoid dehydration.
 Avoid diuretics[water pills] if possible.
 Avoid foods with high content of purines such Red
meat, sugary
drinks,asparagus,cauliflower,spinach,mushrooms,etc.

38. REFERENCES
• Research article
A concise history of gout and hyperuricemia and
their treatment By George Nuki and Peter A Simkin.
• www.niams.nih.gov
• ncbi.nlm.nih.gov

39. THANK YOU