2. Definition
Gout accounts for approximately 5 percent of all cases of arthritis
Caucasian >Negroid peoples
((Particularly those between the ages of 40 and 50))
Rarely seen in children and young adults
3. One theory is that estrogen blocks the anion exchange transporter
in the kidney, causing more uric acid to be excreted in the urine,
and thus lowering the level of uric acid in the blood
4. Hyperuricaemia ((more than 7.0 mg/dl, Normally 3.5 to 7.0 mg/dl))
For people with gout, the uric acid level in the blood is so high that uric acid crystals
form and deposit in joints and other tissues
After several years, the crystals can build up in the joints and surrounding tissues,
forming large deposits, called tophi
Tophi look like lumps under the skin and are often found in or near severely affected
joints
6. Gout with Identifiable Associated Condition
5%
Develops during course of other diseases (Leukaemias,
lymphomas, chemotherapy)
Some drug therapy (Thiazide diuretics, furosamide,
ethacrynic acid and salicylates) and alcohol abuse
Some disorders, Diabetic ketoacidosis, lead poison,
Lymphoproliferative diseases, myeloproliferative
diseases, Hemolytic anemias, psoriasis and renal failure
Dual mechanism
Obesity, Hypoxemia and hypoperfusion
Gout with No Associated Condition
95%
A) Uric acid undersecretion:
80%–90%
Idiopathic
B) Uric acid overproduction:
10%–20%
Hypoxanthine-guanine phosphoribosyl transferase
((HGPRT)) deficiency which is known as “Lesch-
Nyhan syndrome”
Phsphoribosyl pyrophosphate ((PRPP))
synthetase overactivity
7.
8. Drinking too much alcohol
Eating too much of the wrong foods
Crash diet
Surgery
Sudden severe illness
Injury to a joint
chemotherapy
Older age
Male gender and post-menopausal female
Genetic enzyme defects
Purine-riched diet
Hyperparathyroidism
Haemolytic disorders
Myeloproliferative disorders
Lymphoproliferative disorders
Kidney Impairment
Psoriasis
Obesity
Diabetes
Hypertension
High consumption of red meat
Chronic inflammatory diseases
9. Gout usually affects the metatarsophalangeal joint at the base
of the big toe, the Achilles tendons, the olecranon
bursae and the pinnae of the ears. but can also affect other
joints, such as the knee, ankle, heel, foot, hand, wrist and
elbow.
In rare cases, it may later affect the shoulders, hips or spine.
Gout does not spread from joint to joint.
26. In Asymptomatic Gout there is a higher uric acid level in the blood but there are no
symptoms
There can be some back pain related to this
Sometimes tingling sensations can be felt in the foot or other areas
Stage 1
27. Stage 2
Symptoms usually subside within 3 to 10 days or may be longer, with or without treatment
Sudden arthritic attack of joint throbbing pain that worsens progressively, usually occurring at
night or in early morning, followed by warmth, swelling, reddish discoloration or bruising, and
marked tenderness ((even a blanket touching the skin over the affected joint can be unbearable)),
sometimes chills or fever may appear
Bursitis
Most common site of initial attack is the metatarsophalangeal joint
Other sites are ankle, heel, knee, wrist, elbow and fingers
28. Stage 3
Also called Interval Gout
It means the gap between gout attacks with no symptoms and the joints
have no functioning problems
Most people will have a second attack from 6 months to 2 years, while
others are symptoms-free for 5 to 10 years
These delayed attacks can be far more serious than the initial attack and
will move to different areas such as the Achilles Tendon
29. Stage 4
Also called Tophaceous Gout or chalky gout or Polyarticluar Gout
Persistently painful joints with continuous large urate deposits in the cartilages, membranes
between the bones, tendons and soft tissues
Frequency of attacks increases
Skin over the deposits develops sores ((ulcers)) exuding a white pus ((chalky))
Joint stiffness ((limited motion of the affect joint))
Articular cartilage may be destroyed resulting in joint deformities
Patients may develop large Subcutaneous Tophi ((Porous Stones)) in pinna of external ear,
eyelids, nose, around joints, fingers, knees, at the tips of the elbows, tendons, cartilages, soft
tissues as flexors in the forearms and rarely in the vocal cord and around the spine
30. Stage 5
The precipitation of uric acid in the
renal medulla with formation of
characteristic tophi was believed to
evoke an inflammatory response
leading to fibrosis, a loss of
nephrons, and ultimately to the
piece de resistance, chronic
irreversible renal failure
32. Clinical Features
Gout is more likely if:
- Arthritis first appears in the big toe than if it first appears elsewhere
- Onset of symptoms (pain and swelling) takes days or weeks,
symptoms which take hours to develop probably indicate a disorder
other than gout.
- Abnormal enlargements in joints that had been affected by
previous injury or osteoarthritis are possible signs of gout
33. A blood test is usually given for measuring uric acid and
detecting hyperuricemia
A low level of uric acid in the blood makes a diagnosis of gout
much less probable, and a very high level increases the
likelihood of gout
Uric acid levels in the blood during an attack of gout may lie
within or below the normal range
Or
Hyperuricemia may be prevalent in population and doesn’t
necessarily indicate gout
34. Examination of synovial fluid is the most accurate
method for diagnosing gout
Synovial Fluid Analysis ((Joint Fluid Aspiration)):
The sample is examined through a microscope
under polarized light. This special light will reveal
the presence of monosodium urate (MSU) crystals,
which will nearly always confirm a diagnosis of gout
Examination of aspirated joint fluid can rule out
other disorders that mimic gout, such as septic
arthritis and pseudo-gout
35. Is not very useful in diagnosing initial attacks of
acute gouty arthritis
The radiographic findings are generally nonspecific,
consisting of soft tissue swelling around a joint
Bony abnormalities indicate the presence of chronic
gout
In general, gout must be untreated or inadequately
treated for approximately 12 years before chronic
arthritis and bony erosions are seen on radiographs
36. -Joint effusion (earliest sign)
-Preservation of joint space until late stages of disease
-Absence of peri-articular osteopaenia
-Eccentric erosions
-The typical appearance is the presence of well-defined
“punched-out” erosions with sclerotic margins in a
marginal and juxta-articular distribution, with
37. -Punched out lytic bone lesions
-Overhanging sclerotic margins
-Avascular necrosis
-Mineralization is normal
-Tophi: pathognomonic
-Olecranon and prepatellar bursitis
-Peri-articular soft tissue swelling due to crystal deposition in tophi around
the joints is common
-The soft tissue swelling may be hyperdense due to the crystals, and the tophi
can calcify ((uncommon in absence of renal disease)).
38. ACR=AmericanCollegeofRheumatology
-The presence of 6 of the following 13 clinical, laboratory and radiological
features:
1. More than one attack of acute arthritis
2. Maximum inflammation developed within 1 day
3. Mono-arthritis attack
4. Redness observed over joints
5. First metatarsophalangeal joint painful or swollen
6. Unilateral first metatarsophalangeal joint attack
7. Unilateral tarsal joint attack
8. Tophus (proven or suspected)
9. Hyperuricemia
10. Asymmetric swelling within a joint on x-ray/examination
11. Subcortical cysts without erosions on x-ray
12. Mono-sodium urate monohydrate microcrystals in joint fluid
during attack
39. Avoid or restrict foods high in purine ((a substance that produces uric acid when broken down))
These foods include:
Brains, liver, kidneys, tripe, sweetbreads, tongue, shellfish (mussels and oysters), fish roe, scallops,
peas, beans and an excessive amount of red meat
Using of a cane or similar support to keep your weight off that joint
Keep the swollen joint elevated above your chest as much as possible
Ice packs can be helpful in relieving pain and reducing inflammation
Maintaining adequate hydration is key for minimizing attacks and decreasing the formation of kidney
stones
40. Such as acetaminophen (Tylenol) or other more potent analgesics are used to manage pain
1. Colchicine
2. NSAIDS
3. Corticosteroids
Inhibit uric acid synthesis:
Allopurinol, febuxostat ((Uricostatic))
Increase uric acid excretion:
Probencid, Sulphinpyrazone, Benzbromarone ((Uricosuric))
41.
42. Avoiding excessive intake of purine-rich foods
Maintain a healthy body weight
Exercise
Restrict your intake of alcohol, especially beer ((high in Guanosine))
Avoid foods rich in fructose and sucrose which result in hyperuricemia
Avoid diuretic foods or drugs which increase urination
Avoid diet low in potassium ((good sources are tomatoes, potatoes, bananas,
soybeans, brown rice)) since a deficiency increases blood urate
Avoid consuming too much acid-containing substances
Maintain an adequate intake of Vitamin C, since it has been demonstrated to
increase excretion of uric acid
Drink plenty of water to dilute and assist urate excretion
Aviod prolonged exposure to low temperature