7-osteoarthritis and gout

7/31/2019 7-Osteoarthritis and Gout

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DEGENERATIVE JOINTDISEASE:

OSTEOARTHRIT

IS (HYPERTROPHICARTHRITIS)

Michael Roland E. Sumbe


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OSTEOARTHRITIS

Aka degenerative jointdisease (althoughinflammation may be

present) Chronic, nonsystemic

disorder of jointscharacterized by

DEGENERATION OFJOINT CARTILAGEand the formation ofreactive new bone at the

margins of subchondral


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OSTEOARTHRITIS are affected,

incidence increases with age. Also related toobesity and joint trauma

Weigh bearing joints- spine, knees,hips and ends of fingers are most

commonly affected.


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Causes:

1.Primaryosteoarthritis

( a normal part of aging)

Genetic factors (

decreased collagensynthesis)

Chemical factors(drugs such as steroids

that stimulate thecollagen-digestingenzymes in synovialmembrane

Mechanical factors(repeated stress on


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Genetic factors ( decreased collagen synthesis)


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Causes:

2. Secondaryosteoarthritis(follows an

identifiablepredisposing eventthat leads todegenerativechanges)

Trauma (mostcommon cause)

Congenitaldeformity

Obesity


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Clinical manifestations:

Pain aggravatedby use andrelieved by rest

Stiffness of joints HEBERDENS

NODES- bonyovergrowth at

distalinterphalangealjoints : due torepeatedinflammation


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Clinicalmanifestations:

BOUCHARDS

NODES- bonyovergrowth at theproximal

interphalangeal joints

Decreased ROM :due to pain and

stiffness

crepitus: due tocartilage damage
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Diagnosticfindings

1. X-ray: narrowing ofjoint space andmargins

2. Presence ofosteophytes andjoint spacenarrowing:

sensitive andspecific findings

3. Radionuclide bonescan: rule out

inflammatory


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Diagnostic findings

4. MRI: shows affectedjoint, adjacent bonesand disease progression

5. Arthroscopy: showsinternal joint structures

and identifies soft-tissueswelling


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Collaborative management:

Weight loss to reduce extra stress on weight-bearing joints

Exercise to keep joints flexible and improve

muscle strength Heat and cold therapy for temporary pain relief.


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Collaborative management:

Relieve strain and prevent further trauma tojoints: Use cane or walker when indicated

Maintain good posture and body mechanics,avoid excessive weight-bearing andcontinuous standing

Physical therapy to maintain joint mobilityand muscle strength

Promote comfort relief of pain ( analgesicsand NSAIDS)

Joint replacement as needed


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Viscosupplementation theintra-articular injection of hyaluronic

acid. Thought to improve cartilage

function and retard degradation and

have anti-inflammatory effects.

Hyaluronic acid aglycosaminoglycan that acts as alubricant and shock-absorbing fluidin the joint. It stimulates theproduction of synoviocytes,

possibly providing better and moreprolonged pain control

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ASSOCIATED WITH RHEUMATIC

DISORDERS:

GOUT

ARTHRITIS

Michael Roland E. Sumbe


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GOUT ARTHRITIS

Heterogenous group of conditions related to geneticdefect of purine metabolism resulting in

hyperuricemia ( serum concentration greaterthan 7 mg/dL)

Oversecretion of uric acid or renal defect resultingin decreased excretion of uric acid or a combinationof both occurs

Characterized by high levels of uric acid in the bloodand in the urine

There is precipitation of urate crystals ( tophi) inthe joints. This causes inflammation and pain

Occurs most often in males; and it is familial


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Causes:

Genetic defect in purinemetabolism causinghyperuricemia

Retention of uric

acid Combination of the above


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Risk factors: Severe dieting or starvation

Excessive intake of foods highin purines ( shellfish, organmeats)

Hereditary : commonly in

males Medications such as diuretics

and salicylates

Increasing age

Hypertension


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Pathophysiology:

Attacks of gout appear to be related to

sudden decrease or increase of serum

uric acid level

Uric acid becomes supersaturated in theblood and body fluids

Uric acid then crystallizes and forms a

precipitate of urate salts thataccumulates in connective tissuethroughout the body


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Pathophysiology: With repeated attacks,

accumulations of sodium uratecrystal called TOPHI are depositedin the peripheral areas of the bodysuch as great toe, hands and

the ear.

Crystal deposits triggerinflammatory response whenneutrophils begin to ingest them

Neutrophils release lysosomesthatdamage tissues and perpetuatethe inflammation
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Clinical manifestations:

elevated skin

temperature: due to

inflammation

Renal urate lithiasis(kidney stones) with

chronic renal disease

secondary to urate

deposition may

develop


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FOUR clinicaL phases:

1. Asymptomatic hyperurecemia

Serum urate level is elevated even though there

are no symptoms.

2. Acute Gouty Arthritis There is a sudden onset of severe pain in the

great toe or occasionally the heel, ankle, wrist,

fingers and elbows.

When the urate crystals are deposited in the

synovial fluids they can rapidly lyse neutrophils

which release lysosomal enzymes ---

INFLAMMATION


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THE joints become red, hot and tender. The pain

become intense! Fever and elevated WBC.

If untreated, lasts for 3-14 days.

3. Intercritical Gout The intervals between attacks

4. Chronic tophaceous gout Tophi occur in many locations


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MANAGEMENT:

ACUTE ATTACK:COLCHICINE [oral or IV]every 8 hours ( discontinueif diarrhea or nausea andvomiting occur ,or NSAIDs (

Indocin, Butazolidin)Inhibits Phagocytosis of

uric acid crystals byneutrophils

Given until the painsubsides ornauseaand vomiting,cramping or diarrheadevelops


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Immobilization and protection of the

inflamed , painful joints

Local application of heat to stimulate

circulation in the area and clear cellular

debris from the inflammation Local application of cold to decrease pain

Increase fluid intake ( 3L/day) if not

contraindicated to prevent renal calculi NSAIDS to reduce pain and inflammation


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b. CHRONIC

GOUT

Maintenance dosages of

ALLOPURINOL to suppressuric acid formation or control of

uric acid levels, preventingfurther attacks ( used

cautiously with renal failure)

Cholchicine to prevent

recurrent acute attack


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b. CHRONIC GOUT Uricosuric Agents- these are

agents that increases excretion ofuric acid in the urine

Benemid ( Probenecid),Anturane ( sulfinpyrazone)

Zyloprim ( allopurinol)- inhibitsuric acid formation Avoid purine-rich foods ( Organ

meats, shellfish, legumes, sardines,salted anchovies, mushrooms,herring, sweetbreads, beer andwine )


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Nursing interventions in antigout

medications:

Should be used cautiously in clients with GI,

renal, cardiac and hepatic diseases

Maintain a fluid intake of at least 2-3L a day to

avoid kidney stones Instruct client to avoid alcohol and caffeine.

These products can increase uric acid level

Avoid purine-rich foods ( caffeine, alcohol,organ meats, sardines, salmon, scallops and

gravy)


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medications:

Instruct client to take medications with food. To

prevent GI irritation

Instruct client to avoid large doses of vitamin C

while taking allopurinol to prevent kidneystones

Advise client to have yearly eye examination.

Visual changes can occur from prolongedused of allopurinol

Do not take ASA with antigout medications. To

prevent gout hypoglycaemic agents.


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medications:

Observe for the ff. side-effects of antigoutmedications;

Headache

Nausea and vomiting, diarrhea

Bone marrow depression

Flushed skin and skin rash

Uric acid kidney stone

Sore gumsMetallic taste

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