DEGENERATIVE JOINT DISEASE:

OSTEOARTHRIT IS (HYPERTROPHIC
ARTHRITIS)

Michael Roland E. Sumbe

OSTEOARTHRITIS

Aka degenerative joint disease (although inflammation may be present) Chronic, nonsystemic disorder of joints characterized by

DEGENERATION OF JOINT CARTILAGE

and the formation of reactive new bone at the margins of subchondral

OSTEOARTHRITIS

Women and men are equally affected,

incidence increases with age. Also related to obesity and joint trauma Weigh bearing joints- spine, knees, hips and ends of fingers are most commonly affected.

Causes:
1.Primary osteoarthritis
( a normal part of aging) Genetic factors ( decreased collagen synthesis) Chemical factors (drugs such as steroids that stimulate the collagen-digesting enzymes in synovial membrane Mechanical factors (repeated stress on

Genetic factors ( decreased collagen synthesis)

Causes:
2. Secondary osteoarthritis
(follows an identifiable predisposing event that leads to degenerative changes) Trauma (most common cause) Congenital deformity Obesity

Pathophysiolo gy

RHEUMATOID ARTHRITIS- 2.docx videos\Osteoarthritis - Understanding the

Clinical manifestations:
Pain aggravated by use and relieved by rest Stiffness of joints HEBERDENS NODES- bony overgrowth at distal interphalangeal joints : due to repeated inflammation

Clinical manifestations:

BOUCHARDS NODES- bony overgrowth at the proximal interphalangeal joints Decreased ROM : due to pain and stiffness crepitus: due to cartilage damage

Diagnostic findings
1. X-ray: narrowing of joint space and margins 2. Presence of osteophytes and joint space narrowing: sensitive and specific findings 3. Radionuclide bone scan: rule out inflammatory

Diagnostic findings
4. MRI: shows affected joint, adjacent bones and disease progression

5. Arthroscopy: shows internal joint structures and identifies soft-tissue swelling

Collaborative management:

Weight loss to reduce extra stress on weightbearing joints Exercise to keep joints flexible and improve muscle strength Heat and cold therapy for temporary pain relief.

Collaborative management:

Relieve strain and prevent further trauma to joints:

Use cane or walker when indicated Maintain good posture and body mechanics, avoid excessive weight-bearing and continuous standing Physical therapy to maintain joint mobility and muscle strength Promote comfort relief of pain ( analgesics and NSAIDS) Joint replacement as needed

Viscosupplementation the
intra-articular injection of hyaluronic acid. Thought to improve cartilage function and retard degradation and have anti-inflammatory effects.

Hyaluronic acid a glycosaminoglycan that acts as a lubricant and shock-absorbing fluid in the joint. It stimulates the production of synoviocytes, possibly providing better and more prolonged pain control

videos\Osteoarthritis and Rheumatoid Arthritis.avi

METABOLIC AND ENDOCRINE DISEASE ASSOCIATED WITH RHEUMATIC DISORDERS:

GOUT ARTHRITIS
Michael Roland E. Sumbe

GOUT ARTHRITIS

Heterogenous group of conditions related to genetic defect of purine metabolism resulting in hyperuricemia ( serum concentration greater than 7 mg/dL) Oversecretion of uric acid or renal defect resulting in decreased excretion of uric acid or a combination of both occurs Characterized by high levels of uric acid in the blood and in the urine There is precipitation of urate crystals ( tophi) in the joints. This causes inflammation and pain Occurs most often in males; and it is familial

Causes:

Genetic defect in purine

metabolism causing
hyperuricemia

Retention of uric acid

Combination of the above

Risk factors:

Severe dieting or starvation Excessive intake of foods high in purines ( shellfish, organ meats) Hereditary : commonly in males Medications such as diuretics and salicylates Increasing age Hypertension

Pathophysiology:

Attacks of gout appear to be related to sudden decrease or increase of serum uric acid level Uric acid becomes supersaturated in the blood and body fluids Uric acid then crystallizes and forms a precipitate of urate salts that accumulates in connective tissue throughout the body

Pathophysiology:

With repeated attacks, accumulations of sodium urate crystal called TOPHI are deposited in the peripheral areas of the body such as great toe, hands and

the ear.

Crystal deposits trigger inflammatory response when neutrophils begin to ingest them Neutrophils release lysosomes that damage tissues and perpetuate the inflammation

Clinical manifestations:

Joint pain : due to acid deposits and inflammation redness, heat, swelling, great/big toe and ankle are most commonly affected : duet to uric acid deposits and irritation tophi in the great toe, outer ear, hands and feet : due to urate deposits

Clinical manifestations:

elevated skin temperature: due to inflammation Renal urate lithiasis (kidney stones) with chronic renal disease secondary to urate deposition may develop

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

 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

MANAGEMENT:

ACUTE ATTACK: COLCHICINE [oral or IV] every 8 hours ( discontinue if diarrhea or nausea and vomiting occur ,or NSAIDs ( Indocin, Butazolidin)
Inhibits

Phagocytosis of uric acid crystals by neutrophils Given until the pain subsides or nausea and vomiting, cramping or diarrhea develops

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

b. CHRONIC GOUT

Maintenance dosages of ALLOPURINOL to suppress uric acid formation or control of uric acid levels, preventing further attacks ( used cautiously with renal failure) Cholchicine to prevent recurrent acute attack

b. CHRONIC GOUT

Uricosuric Agents- these are agents that increases excretion of uric acid in the urine
Benemid

( Probenecid), Anturane ( sulfinpyrazone) Zyloprim ( allopurinol)- inhibits uric acid formation

Avoid purine-rich foods ( Organ meats, shellfish, legumes, sardines, salted anchovies, mushrooms, herring, sweetbreads, beer and wine )

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)

Nursing interventions in antigout 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 kidney stones Advise client to have yearly eye examination. Visual changes can occur from prolonged used of allopurinol Do not take ASA with antigout medications. To prevent gout hypoglycaemic agents.

Nursing interventions in antigout medications:

Observe for the ff. side-effects of antigout medications; Headache Nausea and vomiting, diarrhea Bone marrow depression Flushed skin and skin rash Uric acid kidney stone Sore gums Metallic taste

videos\Arthritis Gout.avi