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Patho > Musculoskeletal System Healing > Flashcards

Musculoskeletal System Healing Flashcards

1
Q

Tissues of the MSK System

A

Muscle
Bone
Tendon
Ligament
Cartilage

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2
Q

Muscle Strain

A

Tears in muscle fibers
3 Grades

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3
Q

Muscle Strain Grade I

A

Only a few fibers are torn, painful, muscle has complete function

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4
Q

Muscle Strain Grade II

A

Greater Number of fibers torn, severe pain, swelling observed, loss of strength, loss of ROM, bruising may be evident

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5
Q

Muscle Strain Grade III

A

Muscle tears into two separate pieces or is torn away from the tendon, considerable pain and swelling, may be an obvious dent or gap at the site of injury, loss of strength and ROM

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6
Q

Muscle Repair

A

After injury the healing process set up two competitive events:
1. Regeneration of muscle fibers
2. Production of fibrous scar tissue

Phases: Destruction, Repair (Regeneration, Remodeling

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7
Q

Muscle
Destruction Phase

A

After rupture hemorrhage and edema occur
* Degenerative changes and necrosis occur at the site of injury
* An inflammatory reaction is initiated and the necrotic area is invaded
by:
* Macrophages (clear debris)
* T-lymphocytes (release cytokines and growth factors)
* Cytokines and GF’s aid in activation of satellite cells

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8
Q

Muscle
Destruction Phase

A
  • Satellite cells are activated
  • Eventually will transform into myoblastic cells → myotubes → new muscle fibers
  • Formation of a connective tissue scar by fibroblasts occurs at the
    central zone of injury
  • Type III collagen
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9
Q

Muscle
Regeneration Phase

A
  • Begins 3-6 days post injury
  • Peaks at 7-14 days
  • Satellite cells proliferate and differentiate into myoblasts
  • Occurs at both sides of the injury
  • Ultimately form multinucleated myotubes
  • Myotubes attempt to join injured myofibers on the opposite side of
    the injury
  • These regenerating muscle cells begin to pierce through the scar
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10
Q

Muscle
Remodeling Phase

A
  • Tensile strength of healing tissue occurs over time
  • Greater amount of type III collagen
  • The tissue remodels as type III collagen is replaced with type I
  • Collagen cross links stabilize and gain strength
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11
Q

Muscle
Remodeling Phase

A
  • Scar formation, muscle regeneration, orientation of new fibers have
    been enhanced in animal models when subjected to controlled
    movement compared to immobilization
  • Muscle may undergo low-force exercise designed to prevent atrophy and maintain muscle tone
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12
Q

Skeletal muscle pathology
Myasthenia Gravis

A
  • Disorder of the neuromuscular transmission, characterized by fluctuating
    weakness and fatigability of skeletal muscle
  • Peak incidence occurs in women 20-30 years old and men 50-60 years old
    – ratio of women to men is 3:2
  • Autoimmune disease – the presence of specific anti-ACh receptor antibodies, which block the normal binding site for Ach
  • The receptors at the motor endplate are decreased in number and those that remain are altered in shaped resulting in decreased function.
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13
Q

Myasthenia Gravis

A
  • Clinical manifestations are variable from
    mild to severe
  • Include muscle weakness and
    fatigability
  • The fluctuating weakness tends to be
    more evident in the proximal muscles
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14
Q

Myasthenia Gravis

A
  • Cranial muscles (eyelids and muscles
    controlling eye movements) are the first
    to show weakness resulting in diplopia
    (double vision) and ptosis (drooping
    eyelid)
  • Chewing can produce fatigue
  • Difficulty with swallowing can occur
  • Aspiration of food can become
    common
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15
Q

Myasthenia Gravis Tx

A

Acetylcholinesterase inhibitor medication reduces the weakness but does not treat the underlying disease
Administration of the medication is tailored to the individual needs of the
client throughout the
Immunosuppression
using corticosteroids
(prednisone)
~Adverse side effects of using
high doses of corticosteroids
include weight gains,
hypertension, osteoporosis
Plasmapheresis can be used to remove the anti-AChR antibody

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16
Q

Myasthenia Gravis Prognosis

A

Prognosis is variable with periods of remission and exacerbation and the symptoms fluctuate in intensity throughout the day

A severe MG crisis can require mechanical ventilation due to weakness of the respiratory muscles

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17
Q

Muscular Dystrophy (MD)

A
  • Mutation in the gene that creates the protein dystrophin and dystrophin-associated protein complex
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18
Q

Duchenne’s MD (DMD)

A

X-linked recessive (males are affected clinically and females are carriers) with onset at 1-4 years, rapid progression, loss of walking 9-10 years, death late teens.

Severe crippling, Deformities and Contractures

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19
Q

Becker’s MD (BMD)

A

X-linked recessive, onset 5-10 years, slowly progressive, walking maintained past teens, death in 20s

Using hands to push on legs to stand

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20
Q

MD Clinical Manifestations

A
  • Muscular weakness, wasting, hypotonia
  • Child has difficulty getting off the floor
  • Gower’s sign – client places hands on thighs and walks up legs)
  • Frequent falls, difficulty climbing stairs, walks with a waddle gait (proximal
    muscle weakness)
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21
Q

MD Clinical Manifestations Cont’d

A
  • Walks on toes (weakness and contracture of anterior tibialis and peroneals)
  • Increased lumbar lordosis
    (hip extensor weakness)
  • Positive Trendelenburg’s sign (weak hip abductors)
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22
Q

MD Tx

A
  • Treatment – none known to halt progression of disease
    • Treatment is directed at maintaining function in the unaffected muscle groups
      as long as possible.
      * Glucocorticoid therapy (prednisolone)
      tends to slow the progression of the
      disease state.
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23
Q

MD in PT

A

Maintain activity level
Avoid repetition of strenuous activities
Respiratory Monitoring
Provide ambulation/pool therapy for endurance
Info on assistive devices

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24
Q

Bone cells

A
  • Osteogenic cells
    • Develop into osteoblasts
    • Found in the deep layers of the periosteum and bone marrow
  • Osteoblasts
    • Bone formation
    • Found in the periosteum and endosteum
  • Osteocytes
    • Maintain mineral concentration of bone matrix
    • Entrapped in the bone matrix
  • Osteoclasts
    • Bone resorption
    • Bone surfaces
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25
Q

Bone Modeling

A
  • The process by which bones change their shape in response to physiologic influences or mechanical forces
  • May widen or change it’s axis by the removal or the addition of bone in response to biomechanical forces
  • Example – tennis player
  • Cells likely responsible for sensing physical stimuli - osteocyte
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26
Q

Osteocytes

A
  • Bone mass is rapidly lost under unloading conditions
    • Bed rest
    • Local denervation of muscle
    • Hind-limb unloading
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27
Q

Who has higher bone mineral density?

A

Active children and adults

Reduced long-term fracture risk

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28
Q

Bone Remodeling

A
  • Bone is a living organ that undergoes remodeling throughout life
  • In homeostatic equilibrium, resorption and formation of new bone
    matrix are balanced
  • Old bone is continuously replaced by new bone
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29
Q

Bone Remodeling Cont’d

A
  • Activation, Resorption, Formation (ARF)
  • Activation of the osteoclasts
  • Resorption of bone by osteoclasts
  • Formation of new bone by osteoblasts
  • Activated by 3 circumstances
  • Release minerals in response to low serum calcium levels
  • Repair skeletal microdamage
  • Balance the mechanical and mass needs of the skeleton
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30
Q

What are the 3 primary influences affecting this remodeling process?

A

(1) mechanical stresses; (2) calcium and phosphate levels in the extracellular fluid; and (3) hormonal levels of parathyroid hormone, calcitonin, vitamin D, cortisol, growth hormone, thyroid hormone, and sex hormones

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31
Q

Bone - Calcium

A
  • Regulated by parathyroid hormone (PTH)
  • Secreted by the parathyroid gland to
    increase calcium levels
  • Calcitonin
  • Secreted by the thyroid
  • Acts to decrease calcium
  • PTH – stimulates osteoclasts to resorb
    bone, releasing calcium into the blood
  • Calcitonin inhibits the effects of PTH on
    osteoclasts
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32
Q

Bone
Micro-damage

A
  • Main theory for remodeling is the repair of micro-damage
  • Fatigue micro-cracks that occur throughout
    the skeleton
  • Increasing evidence suggests the osteocyte may
    sense micro-cracks in the bone
  • Micro-cracks may cause local osteocyte
    apoptosis
  • Adjacent osteocytes release signaling molecules
  • Studies where apoptosis was inhibited, resorption was diminished
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33
Q

Rickets

A
  • A softening of bones as a result of a deficiency
    or impaired metabolism of vitamin D,
    phosphorus or calcium,
  • Can lead to fractures and deformity
34
Q

Osteoporosis

A
  • Low bone mass and skeletal deterioration
  • Increase susceptibility of fractures
  • Marked increase in bone resorption with rapid bone loss
35
Q

Osteoporosis Incidence/Risk

A
  • Women > men
  • Increased age
  • Body size
  • Family history
  • Post-menopausal
  • Low levels of calcium and vitamin D
  • Low activity level
  • Tobacco and ETOH abuse
36
Q

Osteomyelitis

A

Inflammation of bone caused by an infectious organism such as bacteria, but fungi, parasites, and viruses can also cause skeletal infections (spine, pelvis, and arms/legs often affected)

37
Q

Fracture healing

A
  • Process involving the local response of various growth factors
    and cytokines resulting in the control of osteoclasts and
    osteoblasts
  • Direct or indirect healing pathways
38
Q

Indirect Fx Healing

A

Sequential steps of tissue differentiation, resorption of the surface of the Fx, uniting the Fx fragments by a callus, and long-lasting remodeling

39
Q

Indirect Fx Healing

A
  • Inflammatory phase
    • Initial disruption of bone
    • 3-4 days
  • Repair phase (proliferative phase)
    • 1-4 months
  • Remodeling phase
    • 1-4 years
40
Q

Bone
Inflammatory Phase

A

Hematoma formation
Coagulates around the fracture ends and within the medulla
Forms a template for callus formation

41
Q

Bone
Repair Phase

A

Formation of a cartilaginous callus
-Later undergoes mineralization, resorption, bone replacement
Capillary ingrowth
Fibroblasts transform the hematoma into granulation tissue

42
Q

Bone
Repair Phase Cont’d

A
  • Cartilaginous callus is replaced with
    woven bone
  • At the end of the phase bone union has
    been achieved
  • The structure differs from the original
    bone
43
Q

Bone
Remodeling Phase

A
  • Biomechanic stability has not yet been restored
  • A second resorptive phase initiated
    • Remodels the hard callus into a lamellar bone
      structure with a central medullary cavity
  • Balance of hard callus resorption by osteoclasts and
    lamellar bone deposition by osteoblasts
44
Q

Direct Fx Healing

A

Stable fixation and compression without an apparent callus

45
Q

Direct Fx Healing

A
  • Requires correct anatomical reduction of the fracture
    ends without any gap
  • Often the primary goal of open reduction internal fixation surgery
  • Remodeling of the lamellar bone, Haversian canals, and
    blood vessels
  • Bone on one side of the cortex unites with bone on the other side of the cortex to re-establish mechanical
    continuity
46
Q

Stress Fx

A
  • One of the most common
    overuse injuries
  • Excessive repetitive
    loading without adequate
    periods of rest
    • Increases osteoclast
      activity
    • Osteoblast lag time
  • Intrinsic risks
  • Age
  • Race
  • Gender
  • Extrinsic
  • Malnutrition
47
Q

Tendon Function

A

Transmit force from muscle to bone
Store elastic energy when stretched
Resist passive motions to increase joint stability

48
Q

Effects of age on tendon

A
  • During maturation (<20 years):
    • Cross-links increase
    • Collagen fibril diameter increases
  • Older age (>60 years):
    • Tensile strength and stiffness begin to decrease
      • Decreased collagen content
49
Q

Effects of immobilization on tendon properties

A
  • To maintain the normal mechanical properties of the tendon, there
    must be regular loading
  • Without this, the tendon becomes weaker
    • Collagen content decreases
    • Cross-links decrease
    • Cells and fibers become disorganized
    • Increased deformation with normal tensile loads
50
Q

Acute Tendon Injury

A
  • Injuries caused by sudden loading/excessive force
    • Lacerations
    • Partial thickness rupture
    • Full thickness rupture
  • Compressive forces
  • Repetitive loading/tissue microtrauma
51
Q

Chronic Tendon Injury

A
  • Compressive forces
  • Repetitive loading/tissue microtrauma
52
Q

Ligament Function

A
  • Passive guidance of bones during
    normal function
  • Joint stability during external loading
  • Proprioception
  • Energy conservation
53
Q

Effects of immobilization on ligament
properties

A
  • Load-sensitive structures
  • Immobilization causes a rapid deterioration in strength and stiffness
    • 6-9 weeks = 50% loss in strength and stiffness
    • Bone is also affected by immobilization
  • Leads to atrophy of the ligament
  • Increased cell catabolic activity
54
Q

Effects of exercise on ligament properties

A
  • Loading of a biological tissue stimulates collagen production
  • May increase strength and stiffness of a ligament 10-20%
55
Q

Effects of age on
ligament properties

A
  • Prior to skeletal maturity:
  • Ligaments are more viscous, have a
    smaller cross-sectional area and
    are less stiff.
  • Increased risk for injury at the bony
    insertion
56
Q

Ligaments on Middle age

A

Decreased viscosity, increased
collagen cross-linkages,
decreased elasticity

57
Q

Ligaments in Old age

A
  • Ligaments lose mass, stiffness
    and strength
  • Ligaments more prone to
    excessive creep
  • Joint laxity
  • Changes due to aging process, or
    change in activity? Both
58
Q

Injury to Ligament

A
  • Mechanism of injury (MOI) must involve enough force to rupture collagen fibers
  • Direction of force will dictate if a ligament could be injured
  • Other structures often involved if a ligament has been damaged
59
Q

Ligament Grade I Sprain

A
  • Ligament has been lengthened beyond it’s yield point, but no major damage
  • Pain with stressing the ligament, but no laxity noted
60
Q

Ligament Grade II Sprain

A
  • Ligament has been lengthened with some disruption of ligament fibers
  • Pain with stressing the ligament, some laxity noted
61
Q

Ligament Grade III Sprain

A
  • Ligament has been lengthened with complete or nearly complete disruption of the ligament fibers
  • Significant joint laxity with stressing the ligament, may be an absence of pain
62
Q

Ligament Healing
Bleeding/clotting

A
  • Injury damages the blood supply to the ligament
  • Platelets cause a blood clot to form
  • Fibrin clot leads to vasodilation, infiltration of inflammatory cells
  • Lasts for hours-days (~3)
63
Q

Ligament Healing
Inflammation

A
  • Initiated by fibrin clot formation
  • Macrophages and other inflammatory cells remove debris
  • The process attracts fibroblasts to the area
  • Lasts up to 5 days
64
Q

Ligament Healing
Proliferation/fibroplasia

A
  • Fibroblasts begin to produce a scar matrix
  • Still predominately type I collagen, but a higher amount of types III, V and IV
  • Decrease STIFFNESS and strength
  • While inflammation is still present, scar tissue is more viscous
  • Lasts for up to 6 weeks
65
Q

Ligament Healing
Maturation/remodeling

A
  • Scar matrix contracts
  • Scar tissue behavior is less viscous, more elastic
  • Scar tissue continues to remodel based on the forces applied to the joint
  • Some conversion to type I collagen, but never exactly resembles ligament tissue
  • Alignment of scar tissue fibers dependent on forces applied
  • Lasts up to 12 months post injury
66
Q

Implications for rehabilitation during the inflammatory phase

A
  • Anti-inflammatory modalities may help to limit
    damage to other joint structures and decrease
    pain and swelling
  • Whether or not this influences scar formation is
    unknown
  • Some degree of immobilization may be necessary to allow for the scar tissue to form a “bridge”
    between the two ends of the ligament
67
Q

Implications for rehabilitation during the Proliferative Phase

A
  • Controlled motion is necessary to stimulate adequate scar formation and
    prevent scar tissue adhesions
  • May need to focus on correcting:
  • Altered biomechanics
  • Altered posture/alignment
  • Compensatory movements/postures
68
Q

Implications for rehabilitation during Maturation/Remodeling

A
  • Focus is to continue gradual increase in normal forces to the ligament
  • Promotes improved scar tissue quality
  • Promotes improved alignment of scar tissue fibers
69
Q

Cartilage

A
  • Essentially non-vascular tissue that does not contain nerves
  • Composed of chondrocytes and matrix (collagen, elastin, ground substance)
  • Resistant to deformation and readily withstands compressive forces
70
Q

Articular
(hyaline)
cartilage

A
  • Devoid of blood vessels, lymphatic channels, and innervation
  • Purpose is to distribute joint loads over a wide surface, reducing the stress per unit area
    – Intense stress localization promotes
    cartilage degeneration
    – Abnormal joint articulation increases the stress on the joint surface resulting in
    cartilage failure – leading cause of osteoarthritis
  • Allow movement of opposing joint surfaces
    with minimal friction/wear – fluid film provides
    joint lubrication
71
Q

Nutrition of articular
cartilage

A
  • Cartilage is nourished by synovial fluid contained in the joint
  • This is accomplished by diffusion and the pumping action of the compression and decompression associated with joint
    movement
  • Periods of inactivity (bed rest) at the joint can
    lead to articular cartilage damage
72
Q

Articular cartilage response to injury

A
  • Repair process progresses slowly reflecting the lack of
    vascularization
  • Better repair is evident at the superficial tangential zone and the deep zone
  • Cells of inflammation/repair enter the region via the synovial membrane and pass through the fluid
  • Repair is mediated by chondrocytes and results in fibrocartilage formation
73
Q

Articular cartilage response to injury Cont’d

A
  • Injuries often do not result in adequate repair
  • Surgical repair of articular cartilage often includes drilling into the subchondral bone, inducing vascular damage and initiating an
    aggressive inflammatory response in the bone
    that spills into the cartilage
  • Traumatic damage can include slippage of
    cartilage or the release of cartilage fragments
    from the joint surface
74
Q

Osteoarthritis

A
  • Degenerative joint disease
  • Articular cartilage breaks down because of an imbalance between the mechanical stresses and the ability of the joint structure to handle the loads
75
Q

Osteoarthritis Cont’d

A
  • Mechanical wear and tear leads to gradual breakdown of the articular cartilage
  • As a result, excessive forces are applied to the other parts of the joint
  • Results in narrowing of joint space, sclerosis of the subchondral bone, and osteophyte formation
76
Q

Osteoarthritis Immobilization

A
  • Immobilization can also promote articular cartilage degeneration
    – Articular cartilage is dependent upon repetitive loading/unloading to promote movement of nutrients and wastes
    – Absence of such movement will result in structural weakening of the cartilage
77
Q

Rheumatoid Arthritis (RA)

A
  • Autoimmune induced chronic, systemic
    inflammatory disease resulting in tissue destruction
  • About 80% of individuals with RA are rheumatoid factor positive
78
Q

RA

A
  • Complaints of fatigue, weight loss, weakness, and general diffuse musculoskeletal pain
  • Multiple joints are involved with symmetrical bilateral presentation
  • Joint subluxation and deformity
  • Rheumatoid nodule formation at areas of
    pressure (elbow, Achilles tendon, heart, lung, GI tract
79
Q

RA Diagnosis

A

Exhibits 4 or more of the following:
* Morning stiffness at least 1 hour for 6 weeks
* Swelling in 3 or more joints for 6 weeks
* Swelling of wrist, hand for 6 weeks
* Radiographic evidence of symmetrical joint swelling
* Erosions of bones of hands and decalcification
* Rheumatoid nodules
* Presence of rheumatoid factor

80
Q

RA Tx

A
  • Treatment goals:
  • Reduce pain
  • Maintain mobility
  • Minimize stiffness, edema, joint destruction
81
Q

OA

A

Age of onset: >50
Pain: Worse during or after activity
Stiffness: Worse during or after activity | Usually <30min in morning
Joint characteristics: Hard and bony
Primary joints affected: DIP, CMC of thumb, knees | Not symmetrical
Associated signs: Heberden’s nodes, Bouchard’s nodes

82
Q

RA

A

Age of onset: 30-50
Pain: Inactivity, worse in morning
Stiffness: Worse in the morning | >30 min
Joint characteristics: Soft, tender, warm
Primary joints affected: PIP, MCP, Elbows, ankles, wrists | Symmetrical
Associated signs: Ulnar deviation, Boutonniere deformity, Swan-neck deformity

Patho (13 decks)

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