Gout (apley page 37)

Gout is one of the disease involving presence of the crystal around the joint, bursae and tendons.

Here are the disease similar to gout and their crystal composition

• Gout - Urate crystal depostion disorder


• Peudogout - Calcium pyrophosphate dihydrate (CPPD) deposition disease


• Calcium hydroxyapatite (HA) depostion disorder - Calcium hydroxyapatite

There are 3 main courses of these disease:
1) Become inert and assymptomatic.
2) Acute inflammatory rxn.
3) Slow destruction of t/s.

Generally - disorder of purine metabolism

Characterized by:
1) Hyperuricaemia
2) Deposition of monosodium monohydrate crystal in joint and periarticular t/s.
3) Recurrent attacks of acute synovitis.

Classification
Primary:
- 95%
- Without apparent cause
- d/t under-excretion (majority) and over-production of urate.
Secondary:
- 5%
- Results from prolonged hyperuricemia d/t acquired disorders such as myeloproliferative diseases, administration of diuretics or renal failure.

Sequlae
1) Cartilage degeneration.
2) Renal dysfunction.
3) Uric acid kidney stone.

Epid
- Men:women = 20:1
- Usuallt men >30 y/o
- Often have family h/x of gout.
- Rarely seen before menapause in female.

Pathophysiology
1) Urate crystal deposited in minute clumps in the connective t/s and articular cartilage (commonest sites are the small joints of the hands and feet)
2) They can remain inert for month or years.
3) Possibly as a result of local trauma, the crystal can disperse into the joints and surrounding t/s which excite inflammatory rxn.
4) Clumps or tophi vary in size. It may destroy cartilage and periarticular bone and penetrate the skin.

Common sites
Type of t/s:
- Joints
- Periarticular t/s
- Tendons
- Bursae
Sites:
- Metatarsophalengeal joints of big toe (ada sorang pt hari tu ada swelling and discharge at both feet)
- Finger joints
- Ankle
- Achilles tendon
- Olecranon bursae
- Pinnae of ears

c/f
Acute attack:
- Sudden onset of joint pain which last a week or 2 is typical.
- Maybe spontaneous or aggravated by alcohol, minor trauma, operation, unaccustomed exercise.
- Commonest sites are metatarsophalengeal joints of big toe, ankle, finger joints and olecranon bursa.
- There will be swelling, redness and shiny skin.
- The joint become extreme tender and warm suggesting cellulitis or septic arthritis.
- Sometimes, pt just present with acute pain and tenderness in the heel or the sole of the foot.
Chronic gout:
- Recurrent attack may produce polyarticular gout.
- Tophi may appear around joint, pinna, olecranon. The large one can ulcerate the skin and discharge chalky white material.
- Joint erosion cause stiffness, deformity and chronic pain.
- May present with calculi and renal parenchymal disease.

x-rays
- Acute attack: show soft t/s swelling.
- Chronic attack: asymmetrical, punch out ‘cyst’ in the juxtaarticular bone, joint space narrowing and secondary OA.

Ddx
Psudogout:
- Affect large rather than small joint
- Affect women>men
- Articular calcification on x-ray
- Demonstrating crystal in synovial fluid to confirm dx.
Infxn:
- Cellulitis, septic bursitis, infected bunion.
- Aspiration and synovial fluid exam.
RA:
- Polyarticular gout affecting finger maybe confuse with RA and elbow tophi for rheumatoid nodules.
- Biopsy establish dx.

Rx:
Acute attack:
- Resting joint
- Large dose NSAIDs
- In severe cases, give colchicine
Between attacks:
- Lose wt, cut alcohol, stop diuretics
- Asymptomatic hyperuricemia need no rx.
- Uricosuric (probenecid or sulphinpyrazone) can be used if renal fxn normal.
- Allopurinol usually preferred.
- ! never use these drug in acute attackas it can precipitate the attack.
- ! always use these drug with anti-inflammatory preparation or colchicine.

Hyperuricaemia
- Uric acid in the blood is saturated at 6.4-6.8 mg/dL at ambient conditions, with the upper limit of solubility placed at 7 mg/dL
- Uric acid biosyntesis (refer pic)
- 70% of uric acid from endogenous source while 30% from diet.
- Excreted by the kidey and gut.

link: http://emedicine.medscape.com/article/241767-overview

How is gout treated? (ARTHRITIS FOUNDATION MALAYSIA)
a. For the acute attack

• Non-steroidal anti-inflammatory drugs (NSAIDs) are commonly used to control both the pain and the swelling. They are usually taken in moderate to full doses over a short period of time and are generally efficacious within 2 days. COX II inhibitors are the newer anti-inflammatory drugs which are effective to treat an acute gouty attack. It has less adverse effects to the stomach as compared to the conventional NSAIDs.


• Colchicine has been used for more than 100 years to treat the inflammation caused by gout. Up to six tablets over a 24-hour period usually settle an attack. It is seldom used nowadays to treat acute gout as NSAIDs/COX II inhibitors are more efficacious to settle an attack. Lower doses over a longer period are sometimes prescribed as a preventive measure to reduce the frequency of gout attack when a patient is on uric acid lowering drug.


• Corticosteroids, usually injected directly into the inflamed joint, are used and can control an acute episode efficaciously.


• Each attack should be treated promptly to achieve the best results. If possible tablets should be taken at the very beginning of an attack - if attacks recur - the doctor may give you tablets to keep so you do not have to wait until he/she arrives, or the chemist opens. By following your doctor's instructions carefully and promptly, your attack of gout can be controlled quickly and satisfactorily.
  RememberAlways be on the look-out for the early signs of an attack, because the earlier you start the treatment, the better.

b)Long term To remove contributing factors that raise uric acid level:• Weight control. Being overweight interferes with the body's ability to get rid of uric acid.

• Avoid excessive alcohol. More than one glass of wine or one can of beer a day can raise uric acid levels.

• Diets. Special diets used to be prescribed, but since the effective treatment has been found, most sufferers can eat or drink anything they like. However, certain foods can cause increased uric acid levels. It is sensible to avoid them or reduce the intake. These include liver, brains, kidneys, sweetbreads (pancreas), anchovies, leguminous vegetables, roe, yeast, broths, gravies and sardines. Avoid periods of sudden strict starvation because this can start an attack of gout. Increased consumption of low- fat dairy products can help to reduce uric acid levels.

Remember

• Help yourself by modifying your lifestyle to reduce uric acid • Drink plenty of water

Uric acid lowering drugs
The drugs given to relieve an acute attack have little effect on uric acid levels in the blood. They can do little to prevent further attacks, or stop uric acid being laid down in the joints. Should your attacks become more frequent, or if blood tests show you are accumulating too much uric acid, your doctor may decide to prescribe one of the drugs that reduce the quantity of uric acid in the blood. These have to be taken everyday, whether you have an attack or not, as a preventive measure.

There are now several drugs available that will lower the uric acid level, but it must be appreciated that you may have to persist with the daily treatment for the rest of your life. Should you stop, uric acid will begin to accumulate again.

These tablets are prescribed to be taken regularly. Taken consistently over a period, the treatment ensures that you maintain a normal blood level of uric acid.

The most commonly prescribed tablet is Allopurinol. It reduces the amount of uric acid made by the body. It is well tolerated even when taken for years; the only side-effect that occurs frequently is a rash, which disappears when the tablets are stopped. Occasionally, people may be allergic and have more severe skin rashes.

Sometimes acute attacks of gout may become more common when Allopurinol is started, so it may be necessary to take Colchicine or an NSAID as well. Whichever drug proves right for you, drinking plenty of fluid will help to get rid of uric acid through the kidneys.

Remember

• Allopuritol is not a painkiller • Allopuritol once prescribed means life-time treatment • Do not stop or change the dose of Allopuritol yourself when you have an acute attack.