CAPTURE I

INTRODUCTION

1.1 BACKGROUND

Gouty Arthritis was among the aerlist diseases to be recognized as aclinical entity.

First identified by the Egyptians in 2640 BC, prodagra (acute gout occuring in the first

metatarsophalangeal joint) was later recognized by Hippocrates in the fifth century BC,

who referred to it as ‘the unwalkable diseases’. Some of Hippocrates’ remarkable

clinical perceptions in relation to gout are preserved in aphorisms, which are as true

today as they were 2500 years ago. Hippocrates also noted the link betweenthe disease

and an ‘arthtritis of the rich’, as opposed to rheumatism, an arthritisof the poor. Six

centuries later, Galen was the first to describe tophi, the crystallized monosodium urate

deposits that can follow longstanding hyperuricemia. Galen associated gout with

debauchery and intemperance, but also recognized a hereditary trait that had previously

been referred to by the Roman senator Seneca.

The first person to use the word ‘gout’ to describe podagra (gutta quam podagram

vel artiticam vocant – ‘the gout that is called podagra or arthtritis’) was the Dominician

monk Randolphus of Bocking, domestic chaplain to the Bishop of Chischester (1197-

1258). The term is derived from the Latin word gutta (or ‘drop’), and referred to the

prevailing medieval belief that an excess of one of the four ‘humors’- which in

equilibrium were thought to miantain health – would, under certain circumstances,

‘drop’ or flow into a joint, causing pain and inflammation. Later, gout was described by

Thomas Syndenham, the famous English physician and proponent of hippocratic

medicine, who was himself disabled by gout and renal disease.

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1.2 MAIN PROBLEM

1. What is definition of Gouty Arthritis ?

2. What is etiology of Gouty Arthritis ?

3. What is Signs and Symptoms of Gouty Arthritis ?

4. What is Supporting Check Up of Gouty Arthtritis ?

5. What is Complications of Gouty Arthtritis ?

6. What is Treatments of Gouty Arthtritis ?

1.3 THE PURPOSE OF WRITING

1. To know about definition of Gouty Arthritis.

2. To know etiology of Gouty Arthritis.

3. To know Signs and Symptoms of Gouty Arthritis.

4. To know Supporting Check Up of Gouty Arthtritis.

5. To know Complications of Gouty Arthtritis.

6. To know Treatments of Gouty Arthtritis.

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 CAPTURE II

DISCUSSION

2.1 DEFINITION

Gouty Arthritis is a disease caused by impaired purine metabolism characterized by

hyperuricemia and recurrent acute synovitis attacks (Zairin Helmi, 2011).

Gout is a type of arthritis that causes sudden joint inflammation, usually in a single

joint. Severe gout can sometimes affect many joints at once. This is known as

polyarticular gout.

2.2 ETIOLOGY

Gout is caused by too much uric acid in the bloodstream and accumulation of uric

acid crystals in tissues of the body. Uric acid crystal deposits in the joint cause

inflammation of the joint leading to pain, redness, heat, and swelling. Uric acid is

normally found in the body as a byproduct of the way the body breaks down certain

proteins called purines. Causes of an elevated blood uric acid level (hyperuricemia)

include genetics, obesity, certain medications such as diuretics (water pills), and chronic

decreased kidney function.

2.3 SIGNS AND SYMPTOMS

The characteristic symptoms and signs of gout are

a sudden onset of joint pain,

b joint swelling,

c heat in the affected area, and

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d joint redness.

These symptoms and signs usually affect a single joint. The pain is typically severe,

reflecting the severity of inflammation in the joint. The affected joint is often very

sensitive to touch to the point that some people with gout attacks experience pain from

something as simple as pulling the bedsheets over the inflamed joint. The affected joint

becomes swollen. The medical term for excessive fluid in a joint is a "joint effusion."

Gout frequently involves joints in the lower extremities. The classic location for

gout to occur is the big toe.Podagra is the medical term for inflammation at the base of

the big toe. Gout can also affect the foot, knee, ankle, elbow, wrist, hands, or nearly any

joint in the body. When gout is more severe or longstanding, multiple joints may be

affected at the same time. This causes pain and joint stiffness in multiple joints.

Another sign of gout is the presence of tophi. A tophus is a hard nodule of uric acid

that deposits under the skin. Tophi can be found in various locations in the body,

commonly on the elbows, upper ear cartilage, and on the surface of other joints. When a

tophus is present, it indicates that the body is substantially overloaded with uric acid.

When tophi are present, the uric acid level in the bloodstream typically has been high

for years. The presence of tophi indicates tophaceous gout and treatment with

medications is necessary.

Longstanding untreated gout can lead to joint damage and physical deformity.

Kidney stones may be a sign of gout as uric acid crystals can deposit in the kidney and

cause kidney stones.

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2.4 SUPPORTING CHECK UP

1. Erythrocyte Sedimentation Rate

2. Serum Uric Acid Levels

3. X-ray Joints

4. Uric Acid Levels

2.5 TREATMENTS

1. Non Pharmacological Therapy

a. Adequate Rest

b. Diet

c. Alcohol Control

2. Pharmacological Therapy

For Gouty Arthritis Acute :

a NSAID (Non Steroidal Anti Inflammatory Drugs)

b COX-2 Inhibitor

c Colchicine

d Steroid

For Gouty Arthritis Chronic

a Allopurinol

b Drugs Uricosuric

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2.6 COMPLICATIONS

1. Longstanding untreated gout can cause irreversible joint damage.

2. Uric acid can deposit in the kidneys and cause kidney stones and decreased kidney

function.

3. Uric acid can deposit in the soft tissues, especially around joints, and cause nodules

known as tophi, which can be large and unsightly.

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 CAPTURE III

CLOSING

3.1 CONCLUSION

Gouty Arthritis is a disease caused by impaired purine metabolism characterized by

hyperuricemia and recurrent acute synovitis attacks (Zairin Helmi, 2011). Gout is

caused by too much uric acid in the bloodstream and accumulation of uric acid crystals

in tissues of the body.

3.2 SUGGESTION

We suggest that the government support all the research related to Gouty Arthritis

so we can find a way to cure it not only to reduce it.

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 REFERENCES

Benedict, J. D., Forsham, P. H., Roche, M., Soloway, S., and Stettin, De W., Jr.: The

effect of salicylates and adrenocorticotropic hormone upon the miscible pool of uric

acid in gout, J. Clin. Invest., 29:1104, 1950.

Bishop, C., Garner, W., and Talbott, J. H.: Pool size, turnover rate, and rapidity of

equilibration of injected isotopic uric acid in normal and pathological subjects, J.

Clin. Invest., 30:879, 1951.

Bishop, C., Rand, R., and Talbott, J. H.: The effect of Benemid (p- (di-n

propylsulfamyl) -benzoic acid) in uric acid metabolism in one normal and one gouty

subject, J. Clin. Invest., 30:889, 1951. %