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Clinical Medicine II > Musculoskeletal Pathology & Healing > Flashcards

Musculoskeletal Pathology & Healing Flashcards

1
Q

Tissue/cells capable of some regeneration

A
  • fibroblasts
  • chondrocytes
  • peripheral nerves
  • osteocytes
  • endothelial cells
  • blood cells
  • outer meniscus
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2
Q

Tissue not capable of regeneration (scar)

A
  • cartilage (micro fracture procedure)
  • central nervous system nerves
  • disc
  • inner meniscus
  • cruciate ligament
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3
Q

Define acute injury

A
  • result of a single trauma
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4
Q

Define overuse injury

A
  • involves repetitive stresses associated with prolonged activity
  • repetitive micro trauma exceeds the healing capacity of the tissue
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5
Q

Contributing factors to orthopedic injuries

A
  • weakness
  • poor endurance
  • poor coordination
  • poor aerobic capacity
  • inadequate nutrition
  • insufficient rest/recovery
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6
Q

Injuries to muscle can involve

A
  • strain (partial or complete tear)
  • laceration
  • contusion
  • post exercise soreness
  • compartment syndrome
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7
Q

Where is a strain & overuse injury most common

A
  • myotendinous joint (MTJ)
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8
Q

Characteristics of muscles that are most susceptible to injury

A
  • a greater percentage of Type II fibers
  • two joint muscles
  • muscles subject to high eccentric loading
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9
Q

Healing of skeletal muscle occurs via two competing pathways

A
  • regeneration of disrupted muscle (myoblasts)
  • production of connective tissue scar (fibroblasts)
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10
Q

Define regeneration

A
  • production of newly synthesized tissue that is structurally & functionally identical to the tissue that was traumatized
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11
Q

What can scarring inhibit

A
  • it may inhibit the regeneration of muscle fibers if the formation of granulation tissue is excessive
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12
Q

What occurs during the first 24 hours of muscle healing

A
  • large number of mononuclear cells within damaged muscle cells & in the intercellular connective tissue
  • RBCs & fibrin clots at the site of injury
  • presence of myoblasts
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13
Q

What occurs during 24-48 hours post injury of muscle healing

A
  • marked catabolic response with loss of 27% of total protein
  • most necrotic muscle fragments have been removed (phagocytosis)
  • fibroblasts become prevalent in the connective tissue
  • myoblasts begin to orient along the longitudinal axis of the broken ends of the muscle fibers
  • a hematoma will be noted in the central portion of the injury
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14
Q

What occurs after day 3 of muscle healing

A
  • myoblasts show central nuclei & reorganizing sarcomeres, suggesting the early phase of regeneration
  • increasing my oblast formation & myotubes begin to form
  • muscle protein accumulation begins
  • an intact myofiber may be generated within 7 to 14 days following injury
  • fibroblasts are activated
  • continued phagocytosis (macrophages) of necrotic muscle fibers
  • hematoma still visible histologically
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15
Q

What occurs during days 5-7 of muscle healing

A
  • further progression of regeneration (increased presence of myoblasts & myotubes)
  • significant decline in degree of inflammation
  • central zone of injury: reduces in size & is filled with granulation tissue
  • hematoma small of gone at this point
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16
Q

What occurs after day 14 of muscle healing

A
  • hematoma has resolved
  • young scar tissue
  • a few muscle fibers can be seen traversing the scar tissue that separates the torn muscle fibers within this regenerating zone
  • collagen continues to be laid down
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17
Q

What occurs after the 21 day of muscle healing

A
  • complete repletion of the protein loss
  • diminished evidence of active muscle tissue regeneration & fibroblast activity
  • central zone of the injury all but disappeared, leaving behind a thin connective tissue septum
  • regenerating muscle fibers are now extending across the gap (connective tissue septum) & joining surviving muscle stumps
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18
Q

Muscle healing limitations

A
  • in order to recover normal muscle function following a laceration injury: muscle must regenerate across the repair site & denervated muscle tissue must be reinnervated
  • most denervated fragments remain that way
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19
Q

Define sarcopenia

A
  • age related loss of skeletal muscle mass, function, & ability to regenerate
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20
Q

Theoretical causes of muscle mass loss

A
  • diet & nutrition
  • hormonal change
  • loss of ability to innervate myofibers during healing
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21
Q

How much muscle mass does an adult lose after the age of 70

A
  • 1% of muscle mass per year
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22
Q

Effects of sarcopenia

A
  • loss of muscle mass changes metabolic rate
  • difficulty completing ADLs requiring significant muscle power
  • slow gait speed
  • decreased balance reactions
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23
Q

Define myositis ossificans

A
  • abnormal formation of bone within a muscle following a muscle contusion injury
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24
Q

Symptoms of a myositis ossificans

A
  • prolonged disability
  • severe pain
  • a significant loss of function
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25
Q

Signs of a myositis ossificans

A
  • a large, firm/tender mass within a contused muscle in concert with restricted joint motion
  • plain radiographs will show a soft tissue density at 3 weeks post-injury
  • by 4 to 6 months the bone formation is usually complete
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26
Q

Risk factors of myositis ossificans

A
  • hematoma formation
  • moderate to severe contusion
  • early exercise
  • youth
  • injury to bone or periosteum
  • injury near the musculotendinous junction
  • multiple episodes of injury
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27
Q

Contraindications for myositis ossificans

A
  • aggressive, early activity
  • heat
  • ultrasound
  • massage
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28
Q

Treatment for myositis ossificans

A
  • initial treatment should focus on limiting severity of hemorrhaging
  • rest has been the treatment of choice
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29
Q

What are the limitations to muscle healing

A
  • it won’t get back to 100% but can get close to pre-injury levels, it will take some time
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30
Q

What is the primary function of a tendon

A
  • primary function is to transmit muscle force to the skeletal system
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31
Q

Describe a tendon

A
  • tendons consist of fibroblasts, collagen, and elastin in a ground substance matrix
  • is predominantly type I collagen
  • type III and type V collagen make up about 5% of the tendon
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32
Q

How do tendons heal

A
  • they heal by repair
  • repair is also regeneration
  • a healed tendon is not as strong
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33
Q

Tendon healing inflammatory phase

A
  • neutrophils are the first inflammatory cells to arrive at injury site
  • Day 2 macrophages & lymphocytes are prevalent
  • inflammation has ceased by day 14
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34
Q

Tendon healing proliferative phase

A
  • Days 5-7 fibroblastic activity increases & inflammation decreases
  • developing scar tissue has no significant extracellular matrix for strength & stability (very fragile in this stage)
  • extensive collagen synthesis in the healing tendon
  • type III collagen is produced 1st
  • as healing progresses type III collagen is replaced by type I
  • myofibroblasts are most active from days 5-21
  • Day 21 bundles of collagen fibrils can be seen
  • scar tissue rapidly increases in density up to day 21
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35
Q

Tendon healing remodeling phase

A
  • organization of large quantities of collagen fibrils pool into a compact & parallel system
  • the tensile strength increases as remodeling progresses
  • up through 60 days the scar tissue becomes less cellular & more fibrous
  • vascularity starts to diminish while fibroblast activity remains high
  • restructuring of the collagen network is very active
  • collagen turnover remains high up through day 120
  • 85% of the original collagen in the acute wound stage is replaced with new collagen by day 150
36
Q

Tendon properties & aging

A
  • lower metabolic activity
  • reduction in tendon stiffness (results in altered force transmission from muscle)
37
Q

Define tendinitis

A
  • involves inflammation
38
Q

Define tendinosis

A
  • degenerative
39
Q

Tendinopathy occurs mostly from overuse

A
  • result from sustained activity
  • reparative capacity of tendon is exceeded
  • cellular metabolism altered
  • damage occurs at cellular level, with subsequent injury to the microvasculature
40
Q

Tendon rehabilitation

A
  • modified tension in the line of stress is the optimal stimulus for tendon regeneration
  • wait until 1 week after injury
  • progress slowly
  • careful & controlled passive motion will increase tendon strength & improve the quality of the repair
  • collagen fibers are laid down along lines of mechanical stress
41
Q

What is the effect of mechanical load on the strength of a new scar dependent on

A
  • intensity & duration of the applied load
  • time elapsed since injury
42
Q

Describe a ligament

A
  • short, strong bands of fibrous connective tissue that connects bone to bone
  • 90% type I collagen & <10% type III collagen
  • elastin normally only occupies less than 5% of most skeletal ligaments
43
Q

What is the most common type of ligament injury

A
  • mid-substance tears are more common than avulsion injuries
44
Q
  • Ligament sprain classification
A
  • Grade I: mild pain with no increased laxity
  • Grade II: moderate pain with slight laxity, partial tear
  • Grade III: severe pain with complete disruption of ligament fibers & significant laxity
45
Q

Ligament healing

A
  • hematoma formation & inflammation are followed by relatively slow repair & remodeling phase
  • collateral ligaments are well vascularized & follow classic wound healing
  • final outcome may take over a year
  • pre-injury strength typically not fully recovered (reduced by 30%-50%)
  • ACL heals poorly & without surgery, it will regress or disappear completely (gets most of its nutrition from synovial fluid)
46
Q

What does the quality of ligament healing vary by

A
  • the location of the injury
  • location of the ligament
  • amount of exposure to synovial fluid
47
Q

What are the parts of the joint capsule

A
  • outer layer: stratum fibrosum
  • inner layer: synovial membrane
48
Q

Describe the stratum fibrosum

A
  • dense, rough, fibrous connective tissue with specific areas of thickening (collateral ligaments)
  • helps maintain the joint’s mechanical integrity by securely joining the bones that form the articulation
49
Q

Describe a joint capsule

A
  • menisci, fascia, & other periarticular connective tissues attach themselves to the joint capsule
  • relatively poor blood supply, but a rich supply of nerve fibers
50
Q

Joint capsule sprain classification

A
  • basically the same as ligaments
51
Q

Describe joint capsule injury

A
  • it reacts to trauma with increases in vascularity & fibrous tissue
  • can eventually result in capsular thickening
52
Q

In what ways does joint capsule healing occur

A
  • regeneration of the stratum fibrosum
  • formation of scar tissue (more likely)
53
Q

What are the major functions of the synovium

A
  • lubrication
  • nourishment to avascular articular cartilage
54
Q

Describe the synovium

A
  • covers the inner surface of the fibrous joint capsule & forms a sac enclosing the synovial cavity
  • composed of richly vascularized fibrous connective tissue with lymphatic & nerve supply
  • capable of full regeneration
55
Q

What happens to the synovium following trauma

A
  • increase in synovial fluid volume by 10-20 times the normal
  • increased production of exudate (cells, protein, solid material, & fluid)
  • viscosity (thickness) decreases due to decrease in hyaluronic acid concentration
  • synovium will thicken & synovial fluid will be altered
56
Q

Absorption of fluid & cells from the joint cavity is facilitated by

A
  • active or passive ROM
  • massage
  • intra-articular hydrocortisone
57
Q

The basic inflammatory response in the synovial membrane is

A
  • proliferation of surface cells
  • increase vascularity
  • gradual fibrosis of subsynovial tissue
58
Q

Healing complications of the synovium

A
  • laxity & instability
  • damage to intra-articular inclusions (menisci)
  • the formation of loose bodies in the joint
59
Q

What joints can menisci be found

A
  • radiohumeral
  • acromioclavicular
  • sternoclavicular
  • knee
  • first carpal metacarpal
  • spinal facets
60
Q

Describe knee menisci

A
  • 90% type I collagen
  • blood supply only reaches the outer 25-33%
  • lesions/injuries in avascular regions of meniscus do not regenerate or repair
61
Q

What population do traumatic meniscus tears typically occur in

A
  • usually occur in relatively young athletes or active persons
  • often involve other ligaments
62
Q

What population do degenerative meniscus tears occur in

A
  • degenerative tears are more common in persons 40 years of age or older
  • often associated with degenerative articular cartilage
63
Q

Knee meniscus healing

A
  • healing occurs through repair of the defect with a combination of scar tissue & hyaline like cartilaginous tissue
  • lesion may be filled with dense scar tissue by 10 weeks
  • remodeling of the fibre/vascular scar into hyaline like cartilaginous tissue can take several months
64
Q

Describe articular cartilage

A
  • avascular
  • aneural
  • alymphatic
  • mainly composed of chondrocytes embedded in a matrix of type II collagen, proteoglycans, & non-collagenous protein
65
Q

What kills chondrocytes & disrupts the matrix

A
  • blunt trauma
  • penetrating injuries
  • frictional abrasion
  • sharp concentration of weight bearing forces (contact pressure)
66
Q

What does the healing response of articular cartilage to penetrating injury depend on

A
  • depends on whether the defect lies entirely within the substance of the articular cartilage or extends into subchondral bone
67
Q

What happens during a partially penetrating injury to articular cartilage

A
  • chondrocytes at the site of trauma are killed
  • no inflammation, bleeding, hematoma formation, fibrin clots, or formation of granulation tissue if injury does not penetrate subchondral bone
68
Q

What happens if injury to articular cartilage reaches the subchondral bone

A
  • shows repair by hematoma formation, growth of vascular tissue, migration & proliferation of osteogenic cells, & formation of fibrous tissue or fibrocartilage
69
Q

Articular cartilage injury classification

A
  • Blunt trauma: can penetrate into the subchondral bone
  • Type I defect: superficial laceration does not penetrate into subchondral bone (does not involve injury to blood vessels) & does not involve normal inflammatory & repair components
  • Type II defect: deep, full thickness injury penetrating to the subchondral bone & its blood vessels which elicits an inflammatory response
70
Q

What will a blunt trauma injury result in

A
  • surface loss of proteoglycans
  • cellular degeneration
  • fibrillation (splitting)
  • penetration of the subchondral capillaries into the calcified layer of cartilage
71
Q

Type I articular cartilage injury healing

A
  • necrosis occurs at wound margins together with signs of increased metabolic activity
  • response does not repair the defect & the laceration persists unaltered
72
Q

Type II articular cartilage injury healing

A
  • initial response is formation of a fibrin clot within 48 hours of injury
  • after 1 week fibroblasts & collagen fibers will have replaced the clot
  • after 2 weeks cartilage develops within the fibroblastic tissue as chondrocytes begin to appear in the defect
  • after 1 month most of the fibroblast type cells will differentiate into chondrocytes
  • after 6 months defects still present on cartilage surface
  • after 12 months a majority of the defects initially repaired have degenerated into erosive lesions resembling early osteoarthritis (OA)
  • the defect fills in with weak scar tissue
73
Q

Describe a disc

A
  • the annulus fibrosus (outer layer) consists of alternating oblique layers of collagen fibrils
  • the nucleus pulpous (inner layer) consists of a proteoglycan gel with a water content as high as 88%
  • only the outer portion of the annulus fibrosus has a direct blood supply & has a poor capacity to heal with no regeneration of annular fibers
  • internal disc injuries & internal ruptures of inner annulus fibrosus do not heal
74
Q

Disc injury healing

A
  • a tear in the annulus fibrosus facilitates degeneration of the disc internally
  • may take up to 8 months for granulation tissue to mature, scar, & bridge a defect in the outer annulus fibrosus
75
Q

What are the 4 stages to a disc herniation

A

1) degeneration
2) prolapse
3) extrusion
4) sequestration

76
Q

Effects of prolonged immobilization of muscle

A
  • atrophy
  • decreased strength
  • contracture
  • reduced capillary to muscle fiber ratio
  • reduced mitochondrial density
  • reduced endurance
77
Q

Effects of prolonged immobilization of bone

A
  • generalized osteopenia of cancellous & cortical bone
78
Q

Effects of prolonged immobilization of tendons & ligaments

A
  • disorganization of parallel arrays of fibrils & cells
  • increased deformation with a standard load or compressive force
79
Q

Effects of prolonged immobilization of ligament insertion site

A
  • destruction of ligament fibers attaching to bone
  • reduced load to failure
80
Q

Effects of prolonged immobilization of cartilage

A
  • adherence of fibrofatty connective tissue to cartilage surface
  • loss of cartilage thickness
  • pressure necrosis at points of contact where compression has been applied
81
Q

Effects of prolonged immobilization of synovium

A
  • proliferation of fibrofatty connective tissue into joint space
82
Q

Effects of prolonged immobilization of menisci

A
  • adhesions of synovium villi
  • decreased synovial intima length
  • decreased synovial fluid hyaluronan concentrations
  • decreased synovial intima macrophages
83
Q

Effects of prolonged immobilization of joint

A
  • 0-12: weeks impaired ROM, increased intraarticular pressure during movements, decreased filling volume of joint cavity
  • after 12 weeks: force required for the first flexion-extension cycle is increased more than 12-fold
84
Q

Effects of prolonged immobilization on the heart

A
  • reduced strength of contraction (SV)
  • reduced maximal cardiac output
  • reduced endurance
  • increased work of the heart for a sub maximal load
85
Q

Effects of prolonged immobilization on the lungs

A
  • reduced airway clearance of mucous
  • increased likelihood of pneumonia
  • reduced maximal ventilatory volume
86
Q

Effects of prolonged immobilization on blood

A
  • reduced hematocrit & plasma volume
  • reduced endurance & temperature regulation

Clinical Medicine II (21 decks)

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