NURS 212: Week 15 - Alterations in Musculoskeletal Function

• Alterations in Musculoskeletal Function


  • Bones
  • Fractures
  • Osteoporosis
  • Joints
  • Arthritis
  • Non-inflammatory joint disease (osteoarthritis)
  • Inflammatory joint disease (arthritis)
  • Gout
  • Muscle
  • Fibromyalgia
  • Muscular dystrophy
  • Myasthenia gravis
• Osteoporosis


  Metabolic disease that occurs when the rate of bone resorption is greater than that of bone formation
• Osteoporosis


  • Increased porosity of bone due to loss of bone mass
  • Can be caused by endocrine disorders (ex. Cushing's syndrome) or malignancy
  • Typically caused by loss of estrogen in postmenopausal women
  • Estrogen inhibits osteoclast activity
  • Osteoclast activity increases after menopause, causing net loss of bone mass during remodeling
  • Woman's risk of osteoporosis fracture 1 in 3 after menopause
  • Hormone deficiencies (estrogen, androgen), poor calcium intake, drugs (ex. chronic use of steroids), and lack of weight-bearing exercise are common factors in the rate of bone loss
• Postmenopausal Osteoporosis


  1. Bone density: Reach maximum density at age 30

  2. Lose 0.5% per year

  3. Lose 1% per year postmenopause
• Fracture


  A break in continuity of a bone, an epiphyseal plate, or a cartilaginous joint surface
• Types of fracture


  • Transverse
  • Longitudinal
  • Oblique
  • Spiral
  • Comminuted
  • Greenstick
• Fracture classifications


  • Complete
  • Incomplete
  • Open (compound)
  • Closed (simple)
• Risk factors for fracture


  • Decreased intake or malabsorption of dietary minerals (Ca+, Protein, vitamin C, D, and fluoride)
  • Endocrine dysfunction: by altering calcium and phosphate balance. (PTH, estrogens, corticosteriods)
  • Medications: especially steroids (decrease Ca+ retention)
  • Inactivity: need skeletal stress to preserve bone mass
  • Cigarette smoking: lowers estrogen levels, increases risk for hip fx 50%
  • Alcohol and caffeine: decrease Ca+ absorption 30% (greater risk if > 3 cups /day)
• Repair of bone fracture


  1. Hematoma formation

  2. Fibrocartilage callus formation

  3. Bony callus formation

  4. Bone remodeling
• • Hematoma formation: 1 to 3 days
  • Fibrocartilage formation: 3 days – 2 weeks
  • Callus formation: 2 – 6 weeks
  • Ossification: 3 weeks – 6 months
  • Consolidation/Remodeling: 6 weeks – 1 year
• A fracture is completely healed when clinical healing is achieved. Clinical healing involves: Stable and strong enough to resume its function, Fracture site is free of pain, No gross movement is seen across the fx site
• Complications of fractures


  • Infection
  • Alterations in bone union (delayed union, nonunion, malunion)
  • Fat emboli
  • Nerve damage
  • Compartment syndrome
• Dislocation


  Complete loss of contact between the articular surfaces of two bones
• Subluxation


  Partial loss of joint contact between two bones
• Strains, sprains and avulsions


  • Strain: tearing or stretching of a muscle or tendon
  • Sprain: ligament tears
  • Avulsion: complete separation of a tendon or ligament from its bony attachment site
• Strain and sprain classifications


  • Mild (first degree): Muscle (strain) or joint (sprain) stretched but still stable
  • Moderate (second degree): More tearing with muscle weakness or some joint instability, but incomplete tearing
  • Severe (third degree): Inability to contract the muscle normally (strain) and cause significant joint instability (sprain)
• Pathophysiology of strains and sprains


  1. Inflammation develops between the torn ends

  2. Growth factors direct repair

  3. Collagen formation begins within 4 to 5 days

  4. Healing tendon or ligament requires 4 to 5 weeks but it may take more than 3 months to achieve mechanical stability of a joint

  5. If the site is reinjured during healing, the tendon or ligament may heal in a lengthened shape or with an excessive amount of scar tissue resulting in poor function
• Osteomyelitis


  Acute (<6 wks) or chronic (>6 -8 wks) infection of bone
• Pathophysiology of osteomyelitis


  1. Pus accumulates, pressure within bone cavity increases and blood supply to area diminishes, ischemia and necrosis

  2. Bone cells become necrotic and break off into dead segments called sequestra

  3. Sequestra remain surrounded by pus and become a great medium for spread of bacteria

  4. Bacterial growth results in bone destruction and formation of an abscess. From the abscess cavity, the pus spreads between the trabeculae into the medulla, through the cartilage into the joint, and through the haversian canals of the compact bones to the outside. These sinuses traversing the bone persist for a long time and heal slowly. The pus destroys the bone and sequesters parts of it in the abscess cavity. Reactive new bone is formed around the focus of inflammation.
• Osteoarthritis (OA)


  • Most common, age-related disorder of synovial joints
  • Degenerative joint disease ("wear and tear")
  • Loss of articular cartilage is primary defect
  • Formation of thick subchondral bone and new bone at the joint margins
• Risk factors for osteoarthritis


  • Trauma, sprains, strains, joint dislocations and fx
  • Long-term mechanical stress
  • Inflammation in joint structures
  • Congenital or acquired skeletal deformities
• Pathogenesis of osteoarthritis


  1. Initial injury (wear and tear) releases proteolytic and collagenolytic enzymes from chrondrocytes

  2. Breakdown of the matrix of proteoglycan and collagen

  3. Breakdown of joint integrity leading to degenerative changes

  4. Decreased hydration of cartilage with aging increases likelihood of wear and damage

  5. Microfracture of collagen occurs with stress of weight bearing

  6. Articular surface denudes
• Pathophysiology of osteoarthritis


  1. Structural deterioration of the cartilage

  2. Fissuring, pitting, erosion

  3. Articular surface denudes the full thickness of cartilage

  4. Osteophyte spur formation

  5. Cartilage fragments may break off into joints forming "loose bodies"

  6. Synovium becomes inflamed, secretes
• Risk Factors Osteoarthritis


  • Pathology focuses on load-bearing areas
  • Obesity, joint trauma, stress to joints
  • Common in knees, hips, hands and spine
• Risk factors for osteoarthritis


  • Trauma, sprains, strains, joint dislocations and fx
  • Long-term mechanical stress
  • Inflammation in joint structures
  • Congenital or acquired skeletal deformities
• Pathogenesis of osteoarthritis


  1. Initial injury (wear and tear) releases proteolytic and collagenolytic enzymes from chrondrocytes

  2. Breakdown of the matrix of proteoglycan and collagen

  3. Breakdown of joint integrity leading to degenerative changes

  4. Decreased hydration of cartilage with aging increases likelihood of wear and damage

  5. Microfacture of collagen occurs with stress of weight bearing

  6. Articular surface denudes
• Pathophysiology of osteoarthritis


  • Structural deterioration of the cartilage
  • Fissuring, pitting, erosion
  • Articular surface denudes the full thickness of cartilage
  • Osteophyte spur formation
  • Cartilage fragments may break off into joints forming "loose bodies"
  • Synovium becomes inflamed, secretes increased synovial fluid, joints become distended
• Osteophytes


  A bony outgrowth associated with the degeneration of cartilage at joints
• Signs and symptoms of osteoarthritis


  • Localized joint pain and crepitus with movement
  • Pain and stiffness in the morning <30 min
  • Knees and hips are common sites
  • Improves with movement
  • Pain with function
  • Boney proliferation at joint margins
• Heberden Nodes


  Hard, bony outgrowths seen in the distal interphalangeal joints
• Bouchard Nodes


  Hard, bony outgrowths or gelatinous cysts seen in the proximal interphalangeal joints
• Osteoarthritis affects the distal interphalangeal (DIP) joints
• Rheumatoid Arthritis


  • Systemic inflammatory disease – an autoimmune disease
  • Rheumatoid factor (antibody) reacts with a fragment of IgG to produce immune complexes
  • Immune complexes deposit in synovium initiate inflammation
  • Immune cells attack and destroy cartilage and subchondral bone
• Theories on the etiology of rheumatoid arthritis


  • Infectious antigens (esp. viruses) may trigger the process
  • Autoimmunity: B cells produce rheumatoid factor (RF) antibodies against IgG, immune complexes form and deposit in joints, blood vessels and pleura (systemic)
  • Genetic: certain genetic types such as HLA DR4, HLA DQ, HLA DP have predisposition for RA
• Clinical characteristics of rheumatoid arthritis


  • Ages 40-70s, a juvenile form exists
  • Bilateral symmetric polyarthritis involving small joints
  • Pain and swelling and joint deformities
  • Hands, wrists, elbows, and shoulders
  • Malaise, fatigue, diffuse musculoskeletal pain
  • Finger deformities (Swan-neck and Boutonniere) – metacarpophalangeal (MCP) and proximal interphalangeal (PIP) joint involved, DIP spared
  • Morning stiffness in joints lasting at least an hour before improvement
  • Distal interphalangeal (DIP) joints usually not involved
• Boutonniere deformity


  Finger deformity in rheumatoid arthritis
• Swan-neck deformity


  Finger deformity in rheumatoid arthritis
• Pathophysiology of rheumatoid arthritis


  • Inflammatory cells of the immune system gather in the lining of the joint (called synovium), forming a fibrous layer of abnormal tissue (called pannus)
  • The pannus releases substances that quicken bone erosion, cartilage destruction and damage to the surrounding ligaments
  • Rheumatoid factor against IgG forms immune complexes and initiate inflammation
  • Inflammation leads to formation of a fibrous layer of abnormal tissue known as pannus
  • Inflammation can lead to shortening or rupture of tendons, ligament laxity, joint subluxations, contractures, and deformities
  • Systemic manifestations of inflammation: fatigue, weakness, wt loss, aches/pains
• Rheumatoid arthritis is a systemic autoimmune disease
• Rheumatoid arthritis can be confused with


  • OA, gout, systemic lupus erythematosus (SLE), or other inflammatory disorders