geron musc.skeletal
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MANILA DOCTORS COLLEGECOLLEGE OF NURSING
GERONTOLOGYMUSCULOSKELETAL DISORDERS
Dr. Michael J. Catarroja
Lecturer
Gerontological Nursing 1
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Normal Changes of Aging
Significant alterations causing musculoskeletal
changes in older adults
Human structure Function
Biochemical
Genetic patterns
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Skeleton: Normal Changes of Aging
Two phases of bone loss in normal aging
Type I (menopausal bone loss)
Rapid
Affectswomen
Occurs first 5 to 10 years after menopause
Type II (senescent bone loss)
Slower phase
Affects both sexes after midlife
Phases eventually overlap in women Other conditions may alter signs of normal aging of
skeleton
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Skeleton: Normal Changes of Aging
Bones become
Stiff
Weaker Brittle
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Skeleton: Normal Changes of Aging
Changes in appearance are evident after the
fifth decade.
Height most obvious 20 to 70 years of age
Lose 1 to 2 cm in height every 2 decades
Shortening of the vertebral column
Midlife
Vertebral discs thin
Later years
Decrease individual vertebrae height
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Disproportionate size of long bones of the arm
and legs
Eighth and ninth decades More rapid decrease in vertebral height
Osteoporotic collapse of the vertebrae
Shortening of the trunk with appearance of long
extremities
Skeleton: Normal Changes of Aging
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Skeleton: Normal Changes of Aging
Additional postural changes
Kyphosis
Backward tilt of the head for eye contact Forward bent posture
Hips and knees in flex position
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Muscles: Normal Changes of Aging
Muscle function varies with aging
Trainable into advanced age
Muscle regeneration is normal as age progresses
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Muscles: Normal Changes of Aging
Muscle
Mass
Sarcopenia by age 75
Strength Slow decline
Stamina decreased by age 50
Decreased 65 to 85% of midtwenties by age 80
Tone and tension Decreases after age 30
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Muscle
Size
Decreases causing weakness
Type II muscle fibers
Faster contraction but more atrophy
Type I
Slower contraction and less atrophy
Help maintain posture
Help perform repetitive exercise s
Shape Distinct
More prominent
Muscles: Normal Changes of Aging
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Routine daily activities keep the upper
extremities functioning better than walking.
Muscles: Normal Changes of Aging
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Cartilage
Hyaline cartilage (joint lining)
Normally lines joints
Erodes and tears with advancing age
Causes bone to bone contact
Knee cartilage
Experiences normal wear and tear
Thins about 0.25 mm/year
Discomfort and slow joint movement
Diminished joint lubricant
Nonarticular cartilage (ears and nose)
Grows throughout life
Joints, Ligaments, Tendons, and Cartilage:
Normal Changes with Aging
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Ligaments, tendons, and joint capsules
Lose elasticity
Less flexible Joint ROM decreases
Joints, Ligaments, Tendons, and Cartilage:Joints, Ligaments, Tendons, and Cartilage:
Normal Changes with AgingNormal Changes with Aging
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Osteoporosis
Most common metabolic disease
Characterized by low bone mass and deterioration
of bone tissue.
Bone strength is compromised increasing risk for
fractures.
Affects 50% ofwomen during their lifetimes
20 million women and 8 million men diagnosed in
the United States
3.8 million women receive adequate care
Metabolic Bone Diseases
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Osteoporosis
High risk factors for osteoporosis
Increased age
Female sex White or Asian race
Positive family history
Thin body habitus
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Osteoporosis
Additional risk factors for osteoporosis
Low calcium intake
Prolonged immobility Excessive alcohol intake
Cigarette smoking
Long-term use of corticosteroids, anticonvulsants,
or thyroid hormones
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Reduced BMD Highly predictive of spinal and hip fractures
Osteoporotic fractures affect 1.3 million per yearin the United States
Vertebrae fractures affect about 500,000 peopleper year
Hip and wrist fractures affect about 260,000 peryear
One in five patients die within 1 year
One third regain their prefracture mobility andindependence level
Pathophysiology of Osteoporosis
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Classification of Osteoporosis
Primary osteoporosis
Type I (menopausal bone loss)
Type II (senescent bone loss)
Secondary osteoporosis Hyperparathyroidism
Malignancy
Immobilization
Gastrointestinal disease
Renal disease
Drugs causing bone loss such as vitamin D deficiencies andglucocorticoids
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Menopausal Bone Loss
(Type 1)
Before menopause, sex hormones protect from bone
loss.
After menopause
Overproduction of IL-6
Up to tenfold loss of bone mass
Resorption (loss of bone matrix) more than deposition (rapid bone
growth)
Susceptible women close to age 70 can lose 50% ofperipheral cortical bone mass
Cause of vertebral and Colles' fractures
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Senescent Bone Loss
(Type 2)
Decreased amount of bone during remodeling
Occurs in both sexes
Caused by aging
Decreased trabecular (cancellous) bone wallthickness
Decreased osteoblast formation
Decreased bone mineral density
Decreased rate of bone formation Cause of vertebral and hip fractures
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Trajectory of Bone Loss for Women
Lower peak bone mass than men
Less in the "bone bank because of thinner bones
Lose bone mass with lactation
Rapid withdrawal from "bone bank" duringperimenopause
Longer life span increases risk for osteoporosis
Signs/symptoms usually absent
First sign is often a fracture
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Pharmacology and Nursing
Responsibilities for Osteoporosis
Antiresorptive therapy
Preserves or increases bone density
Decreases rate of bone resorption
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Pharmacology and Nursing
Responsibilities for Osteoporosis
Classifications and special considerations
Bisphosphonates (alendronate [Fosamax] and
risendronate [Actonel])
Inhibit osteoclastic activity
Decrease postmenopausal vertebral and nonvertebral fractures by
40 to 50%
Adverse gastrointestinal symptoms
Esophageal irritation, heartburn
Difficulty swallowing
Do not take calcium with bisphosphonates interferes with
absorption
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Pharmacology and Nursing
Responsibilities for Osteoporosis
Selective estrogen receptor modulators (SERMs) Provide benefits of estrogens without the disadvantages
Raloxifene approved for postmenopausal prevention andtreatment of osteoporosis in women
SERMS less effective than bisphosphonates
Calcitonin Safe but less effective treatment for osteoporosis
Decreases spinal fractures by up to 35%
Hormone replacement therapy (HRT)
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OSTEOARTHRITIS
Gerontological Nursing 26
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Primary or Idiopathic Osteoarthritis
No single, clear cause
Group of similar disorders
Involve complex biomedical, biochemical, andcellular processes
Changes in several joints as a result of various
causes
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Secondary Arthritis
Secondary arthritis involves
An underlying condition
Trauma
Bone disease
Inflammatory joint disease
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Pathophysiology
Progressive erosion of joint articular cartilage
Formation of new bone in joint space
Involved joints
Hands Weight bearing joints of the knees and hips
Central joints of the cervical and lumbar spine
How does this happen?
Cartilage thins underlying bone (subchrondal bone) is no
longer protected
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Cartilage not available to buffer
Subchrondral bone becomes irritated
degeneration of the joint bone hypertrophy
bony spurs (osteophytes) growth and
enlargement contours of the joint
Small pieces may break off (joint mice) irritate
the synovial membrane
joint effusion
limitedmovement
Pathophysiology
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Clinical Manifestations
90% of all people have x-ray evidence of primaryosteoarthritis in their weight-bearing joints by age 40.
OA symptoms 40% of people with severe OA have pain
Most common symptoms Earlymorning stiffness resolving in 30 minutes
Joint pain Occurs during activity
Relieved by rest
With progressive disease
Pain may be present at rest Interrupt ion of sleep patterns
Source of pain may be unknown, but it needs to be identifiedin order to provide treatment
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Joint involvement
Asymmetrical at first
Bony appearance of joints
Crepitus (a grating sound on movement)
Range of motion deficit
Muscle weakness
Clinical Manifestations
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Hands
New bone growth
Heberdens nodes (DIPdistal interphalangeal joint)
Bouchards nodes (PIPproximal interphalangeal joint) Pain with active and passive motion
Joint damage + chronic pain + muscleweakness impaired balance + decreased
activity
Clinical Manifestations
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Pharmacology and Nursing
Responsibilities for Osteoarthritis
No therapywill slow or halt progression
Current therapy directed at relief of pain andminimizing functional disability
Agents for pain relief for OA NSAIDs
Topical agents Capsaicin nonprescription drug
Prevent the reaccumulation of substance P (a
neurotransmitter) in peripheral sensory neurons Applied 2 to 4 times daily to affected area
May cause heat or burning
Relief may require up to 4 to 6 weeks of applications
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Systemic oral agents
Acetaminophen (Tylenol)
First line pharmacological therapy
Give up to 4 gm/daywith minimal toxicity
Higher doses may cause liver damage
Ceiling effect = increasing the dose does not increase
the analgesic benefit Use alone or as an adjunct to
NSAIDs
Pharmacology and Nursing
Responsibilities for Osteoarthritis
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Nonsteroidal anti-inflammatory drugs
(NSAIDs)
Most common treatment for pain and
inflammation of OA
COX-2 inhibitors, a new category of anti-
inflammatory drugs
Considered safe for the GI tract Side effects include renal impairment (see RA section)
Pharmacology and Nursing
Responsibilities for Osteoarthritis
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Adjuvant agents
Intra-articular agents
Corticosteroids valuable for synovial inflammation
Synovial effusion removed prior to injections
Limited to 4/year in any one joint
Hyaluronic acid
Normal component of the joint for lubrication and nutrition
Decreased pain for longer periods than other intra-articulartherapies
Administered in series of 3 to 5 injections
Pharmacology and Nursing
Responsibilities for Osteoarthritis
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Selected Diagnostic Tests and Values for
Musculoskeletal Problems
Bone mineral density test (BMD)
Dual energy x-ray absorptiometry (DEXA)
Proximal femur predicts hip fracture risk best
Gold standard for fracture prediction Other sites tested include spine, wrist, or total body
Results
Compared with young adult mean
Or compared norm group of same age
BMD 1 SD belowmean (-1 S) = osteopenia
BMD 2.5 SD below mean (-2.5 SD) = severe osteoporosis
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Bone mineral density test (BMD)
Pitfalls
Bone changes also the result of arthritis or disk disease
in lumbar spine
ArbitrarySD cutoffs to determine diagnosis
Results varywith technique and patient position
Current criteria based on postmenopausal white
women
Selected Diagnostic Tests and Values for
Musculoskeletal Problems
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Bone and Joint Radiography
X-ray use
Diagnose and stage rheumatic diseases
Diagnose fractures
Detect musculoskeletal structure, integrity,
texture, or density problems
Evaluate disease progression and treatment
efficacy
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Computed tomography (CT)/magnetic
resonance imaging (MRI)
Visualize
Inflammation
Musculoskeletal changes
Synovitis
Edema Bone bruises
Occult fractures and articular damage
Bone and Joint Radiography
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Computed tomography (CT)/magnetic resonanceimaging (MRI) Advantages
Uses a large magnet and radio waves to produce energy field
Detailed image Does not use radiation or a contrast medium
Disadvantages More expensive
Requires special facilities
Cannot show calcification or bone mineralization Client hears soft to thunderous noises and may use earplugs
Bone and Joint Radiography
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Bone Scan
Detects skeletal trauma and disease
Determines degree bone matrix takes up
radioactive isotope
Determines reason for an elevated ALP
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Blood Serum Tests
Electrolytes: calcium level
Bone and muscle enzymes: alkalinephosphatase (ALP)
Joint tests
Rheumatoid factor (RF)
Acute phase reactants
C-reactive protein (CRP) Erythrocyte sedimentation rate (ESR)
Serum uric acid (SUA)
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Special considerations
Electrolytes: serum calcium and phosphorus
decreased in the older person
Calcium
Increased in Pagets disease, with bone fractures, and
with immobility
Decreased in osteoporosis and osteomalacia
Serum calcium (normal range older adult 8.8 to 10.2
mg/dl)
Blood Serum Tests
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Special considerations
Phosphorus
Phosphorus (normal range for older person > 60 = 2.3
to 3.7 mg/dl)
Increased in bone fractures and healing state
Decreased in osteomalacia
Serum Uric Acid (SUA)
Diagnosis of gout is not established unless SUA is found
in tissue or synovial fluid
Blood Serum Tests
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Acute phase reactants C-reactive protein (CRP) anderythrocyte sedimentation rate (ESR) Erythrocyte sedimentation rate
Most common measurement of acute phase proteins in rheumatic
disease Direct relationship to acute phase proteins
Results in 1 hour
C-reactive protein Acute phase reactant determines presence of inflammatory
process Bacterial infection or rheumatic disease
Increases and returns to normal quicker than ESR
Blood Serum Tests
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Alkaline phosphatase (ALP)
Enzyme associated with bone activity
Normal values: men = 45 to115 U/L, women = 30 to 100
U/L Values increase after age 50
Identify increases in osteoblastic activity and inflammatory
conditions
Elevated with Pagets disease (> 5x normal)
Isoenzymes ALP1 (liver origin) and ALP2 (bone origin)
determine if elevation is bone disease
Blood Serum Tests
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Lifestyle Changes
Increase in exercise
Weight loss
Eating healthy diets Healthy People 2010
(www.health.gov/healthypeople)
Nations goals and objectives for improved health
Includes an objective for arthritis patient
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Additional Nonpharmacological
Strategies
Additional nonpharmacological strategies to enhance
comfort with OA
Apply heat to painful joints
Use cold applications to reduce pain and swelling Use canes, crutches, and walkers to protect joints
Use assistive technology
Maintain, increase, or improve function
Commercial purchase or custom made
Available for general daily living, home management, school, and
work activities
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