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Assessment & Management For The Patient

With chronic Musculoskeletal System


Disorders

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Session objectives

 Upon completion of this System, the students


should be able to:
– Identify joint and connective tissue disorders
with their respective causes, c/m, pp and
management
– Describe metabolic bone disorders
– Implement nursing process for all disorders

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Joint & Connective Tissues
Disorders

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Rheumatoid Arthritis

 A chronic systemic disease characterized by recurrent


inflammation of diarthrodial joints and related structures

 Onset can be acute or insidious

 Characterized by periods of remissions and exacerbation.

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Rheumatoid Arthritis
Etiology C/M

 Infection  Nodules
 Autoimmunity  Arteritis
 Genetic  Neuropathy
 Scleritis
 Pericarditis
 Lymphadenopathy
 Splenomegaly

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Rheumatoid Arthritis (Lab Dx)

 Elevated Erythrocyte Sedimentation Rate (ESR)


– reflects inflammatory activity
 Elevated Rheumatoid Factor (RF)
– Measures the presence of unusual IgG and IgM.
 Anemia (Decreased RBC)
 C-Reactive protein (CRP) and antinuclear antibody (ANA) may
also be positive
 Arthrocentesis
– Needle aspiration of synovial fluid: fluid is cloudy, milky, or
dark yellow, containing WBCs

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Rheumatoid Arthritis (Management)

 Pharmacologic Therapy (Disease modifying drugs)


– Methotrexate, 7.5mg P.O., once per week. Increase dose gradually
to a maximum of 25mg per week. Plus
– Folic acid 5mg P.O., per week with methotrexate at least 24 hours
after the methotrexate dose. OR/Plus
– ChloroQuine phosphate, 150mg P.O., (as base) daily for 5 days of
each week for 2–3 months. OR
– SulfasalaZine, 500mg P.O., 12 hourly.
 Oral corticosteroids:
– Prednisolone, 40mg P.O., daily for 2 weeks during acute flares

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Rheumatoid Arthritis (Management)

 NSAIDs:
– Ibuprofen, 800mg, P.O.,TID with meals. Or
– Diclofenac, Immediate or delayed release tablet: 150-
200mg/day P.O., in 2-4 divided doses.
– Indomethacin, 25-50mg P.O., BID TO TID; maximum
dose: 200mg/day.
 Nutritional: weight control,
 Reconstructive Surgery

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Rheumatoid Arthritis (Management)

 Rest and Activity


– Naps, avoid over-exertion
– Avoid positions of flexion
– Energy conservation
– Exercise therapy – for flexibility, strength, endurance, to
maintain joint mobility/function
 Joint protection
– Splints for acutely inflamed joints
 Cold therapy – for inflammation during flare-ups
 Heat therapy – for chronic stiffness

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Gouty Arthritis

 Most common inflammatory arthritis in elderly


– Increasing prevalence with age (75-85 years high)
– Men > women, (for < 65years)
 Deposition of urate crystals in tissue
 Gout in women
– Usually > 65 years.
– Loss of estrogens induced uricosuric effect

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Gouty Arthritis (Risk factors)

 Purine rich foods & nutritional supplements (animal


product consumers)
 Some drugs (low dose aspirin, thiazides, niacin,
pyrazinamide, ethanbutol….)
 Obesity & excessive weight gain
 Moderate to heavy alcohol intake, high BP
 Abnormal kidney function

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Gouty Arthritis (Management)

NSAIDs:
 Aspirin up to 500mg
 Ibuprofen up to 800mg
 Indomethacin 25-50mg
Corticosteroids:
 prednisone 30-40 mg/d for 5 days
 Prednisolone 5mg
 Bethamethasone 6mg/ml
 Methylprednisolone 16-32 mg
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Osteomyelitis

 Is an infection of the bone that becomes


infected by one of the three modes.
– Extension of soft tissue infection (e.g. Vascular
ulcer, incisional infection)
– Direct bone contamination from bone surgery, or
traumatic injury (e.g gun shot)
– Hematogenous spread from other sites of infection
(e.g. upper respiratory infections).

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Osteomyelitis (C/M)

 painful,
 swollen and
 extremely tender
Osteomyelitis (lab Diagnosis)
 Elevated leukocyte levels and elevated sedimentation rate.
 Wound and blood culture studies
 Standard x-ray studies

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Osteomyelitis (Management)
 Antibiotic therapy for 3-6 weeks.
– Amoxicillin-clavulanate 875 mg/125 mg PO Q12h or.
– Ciprofloxacin 750 mg PO Q12h plus clindamycin 300-450 mg PO
Q6h or.
– Levofloxacin 750 mg PO daily plus clindamycin 300-450 mg PO q6h.
 Supportive measures such as hydration, high protein & vitamins.
 Immobilize the affected area to prevent pathogenic fracture.
 Internal fixation or external supportive device may be need.

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Metabolic Bone Disorders

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Loss of bone exceeds rate of
bone formation which
usually increases in older
women, white race and null
parity.

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Osteoporosis

C/M:
 Mostly ‘silent disease’ b/c of lack of s/sx
 Bone pain,
 Decrease movement
 Easily breakable bones
 Ominous/worrying signs: pain in lower back,
deformity, kyphosis, loss of height, markedly aged
appearance

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Osteoporosis (Classification)

 Generalized osteoporosis occurs most commonly in


postmenopausal women and men in their 60s and
70s……primary osteoporosis (because of
inadequate intake or absorption of calcium, estrogen
deficiency, and sedentary life)
 Secondary osteoporosis results from an associated
medical condition such as hyperparathyroidism,
long-term drug therapy, long-term immobility.
 Regional osteoporosis occurs when a limb is
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Osteoporosis diagnosis methods

 X-rays
 CT – scans
 Serum calcium, phosphorous and alkaline
phosphatase levels,

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Osteoporosis (Management)

Thereis no cure! But as a supportive


management:
 Calcium.. … to enhance bone strength
 Vitamin D … to support bone metabolism
 Estrogen replacement… to decrease bone resorption
 Estrogen with progestin …
 SERM (Selective Estrogen Receptor Modulator) with anti-
estrogens

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Osteoporosis (Management)

 Exercise

 Avoid caffeine intake


 Improve protein, K,..intake
 Providing hazard free environment to avoid fall
 Safety for pathologic fracture (Health education)

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Osteomalacia

 Softening of the bone tissue characterized by


inadequate mineralization of osteoid.
Causes:
 Lack of activated Vitamin D (this results in poor
utilization of calcium and phosphorous)
 Hyperparathyroidism leads to skeletal decalcification
and thus to osteomalacia by increasing phosphate
excretion in the urine.
 Prolonged use of antiseizure medication (phenytoin,
phenobarbital) poses a risk for osteomalacia, as does
insufficient vitamin D (dietary, sunlight).

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Osteomalacia

 Osteomalacia may result from failed calcium absorption


(malabsorption syndrome) or from excessive loss of
calcium from the body.
 Gastrointestinal disorders (eg, celiac disease, chronic
biliary tract obstruction, chronic pancreatitis, small bowel
resection) in which fats are inadequately absorbed
 In addition, liver and kidney diseases can produce a lack
of vitamin D because these are the organs that convert
vitamin D to its active form.

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Diagnosis method of osteomalacia

 X-rays
 CT – scans
 Serum calcium, phosphorous and alkaline
phosphatase levels,

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Osteomalacia

C/M: easily breakable bones,


Management:
vitamin D from exposure to sunlight
Nutritional / proteins, minerals/
Physical, psychological, and pharmaceutical
measures are used to reduce the patient’s
discomfort and pain.

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