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Physical Agents > Inflammation & the Healing Process > Flashcards

Inflammation & the Healing Process Flashcards

1
Q

Primary Injury

A
  • Macrotrauma and Microtrauma
  • Ultrastructural changes
  • Swelling
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2
Q

Macrotrauma

A

large injury that results in failure of musculoskeletal structures

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3
Q

Microtruama

A

Overuse, cyclic loading, friction injuries. Small stresses cause injury overtime

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4
Q

Primary injury causes

A
  • Physical agents ( force, burns, radiation)
  • Metabolic processes (ischemia, hypoxia)
  • Biological agents (bacteria, parasites)
  • Chemical agents (acids, chemicals)
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5
Q

Secondary Injury

A

Cells that were not injured in the primary injury become injured because of this process

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6
Q

Secondary injury: Enzymatic injury

A

Lysosomal mechanism

- cell membrane destroyed and everything within it released including lysosomes which eat tissue

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7
Q

Secondary injury: metabolic injury

A
  • Ischemia > hypoxia > inadequate fuel > inadequate waste removal
  • Membrane permeability mechanism
  • Mitochondrial mechanism
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8
Q

Inflammation

A

A coordinated, complex, and dynamic series of events that develops as a result of trauma or injury to vascularized tissue

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9
Q

Cardinal signs of Inflammation

A
  • Heat (calor)
  • Redness (rubor)
  • Swelling (tumor)
  • Pain (dolor)
  • Loss of function ( functio laesa)
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10
Q

Cause of heat

A

increased vascularity

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11
Q

Cause of Redness

A

Increased Vascularity

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12
Q

Cause of Swelling

A

blockage of lymphatic drainage

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13
Q

Cause of pain

A

Physical pressure and/or chemical irritation of pain sensitive structures

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14
Q

Cause of loss of function

A

Pain and swelling

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15
Q

Phases of tissue injury and repair

A
  • Hemostasis (immediate sec/min)
  • Inflammatory stage (days 1-6)
  • Proliferation stage (Days 3-10)
  • Maturation Stage ( day 9 on)
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16
Q

Hemostasis phase vascular response

A

Vasoconstriction in injured vessels

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17
Q

Hemostasis phase hemostatic response

A

Controls blood loss

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18
Q

Inflammatory Phase characteristics

A
  • Vascular changes
  • exudate of cells and chemicals
  • Clot formation
  • Phagocytosis
  • Neutralization of irritants
  • Early fibroblastic activity
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19
Q

Inflammatory phase Clinical Signs

A
  • Inflammation
  • Pain before resistence
  • Tender to Palpation
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20
Q

Inflammatory phase impairments

A
  • Pain
  • Edema
  • Muscle Spasm
  • reduced AROM/PROM
  • Joint effusion
  • Decreased use of associated areas
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21
Q

Inflammatory phase vascular response

A
  • Dilation of non-injured vessels in area of trauma
  • mediated by histamine, hageman factor, bradykinin, prostaglandins, and complement fractions
  • allows leukocytes into injured area -eat up junk
  • neutrophils migrate to injured area
  • line the endothelium of vessels (migration)
  • lay down in layers (pavementing), mediated by fibronectin
  • squeeze through vessel walls (diapedesis)
  • move from inside to outside blood vessl (extravasation)
  • migrate from blood vessels to parivascular tissue (emingration)
  • **Allows protein-rich fluid to escape into tissues
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22
Q

Swelling

A

accumulation of fluid within extravascular space and interstitial tissues

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23
Q

Hemmorrhaging

A

Due to damaged vessels

  • Blood accumulated in tissue= hematoma
  • Blood accumulated in joint= hemarthrosis
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24
Q

Edema

A

Fluid portion of blood in tissues

  • due to changes in fluid dynamics
  • proteins attract water- draws plasma out of vascular tissue
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25
Q

Capillary filtration Pressure equation

A

CFP= (CHP + TOP) - (THP + COP)

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26
Q

CHP

A

Capillary hydrostatic pressure

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27
Q

TOP

A

Tissue osmotic pressure

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28
Q

THP

A

Tissue hydrostatic pressure

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29
Q

COP

A

Capillary osmotic pressure

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30
Q

hydrostatic pressure

A

pressure exerted by a column of water (pushes water)

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31
Q

osmotic pressure

A

pressure resulting from attraction of fluid by free proteins (pulls water)

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32
Q

Changes in Capillary filtration pressure (CFP) after injury

A
  • TOP increases
  • Pulls fluid into tissues
  • edema and swelling results
  • but initial swelling after injury from hemorrhaging
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33
Q

Erythrocyte response to injury- inflammatory stage

A

play minor role in inflammatory process

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34
Q

Leukocyte response to injury- inflammatory stage

A
  • clear injured area of debris and microorganisms

- set the stage for tissue repair

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35
Q

Cellular response: first 24 hours

A

Polymorphonuclear leukocytes

  • Neutrophils
  • Basophils
  • Eosinophils
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36
Q

Neutrophils

A
  • pagocytosis

- release enzymes (protease) & collagenolytic enzymes (collagenases)

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37
Q

Basophils

A
  • release histamine
  • contribute to increased vascular permeability
  • apply cold= decrease amt of histamine= vasoconstriction
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38
Q

Eosinophils

A

Phagocytosis

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39
Q

Cellular response: first 24-48 hrs

A

Mononuclear leukocytes

  • Monocytes
  • Lymphocytes
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40
Q

Monocytes

A
  • converted into macrophages
  • collagenase
  • fibronectin
  • hydrogen peroxide, ascorbic acid, lactic acid
  • Most effective in oxygen rich environment in tissue
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41
Q

Lymphocytes

A

Supply antibodies

- mediate immune response

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42
Q

Immune response to injury

A
  • B lymphocytes
  • T lymphocytes
  • Activation of complement system
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43
Q

immune response: B lymphocytes

A

release antibodies into bloodstream

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44
Q

immune response: T lymphocytes

A

Assist B cells in regulation of cloning

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45
Q

immune response: activation of complement system

A

Series of enzymatic plasma proteins

  • increased vascular permeability
  • stimulate phagocytosis
  • act as chemotactic stimuli for leukocytes
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46
Q

Metabolic response to injury

A

Hypoxia: cell deprived of oxygen (lack of blood supply)
- switches from aerobic to anaerobic metabolism-glycolysis-glucose conversion to lactic acid
-Decreased ATP production
-Decreased cell membrane function
*Na+ pump slows or stops> [Na+] inside cell increases>
&raquo_space; increased cellular H20> cell swells> burst or die
- increased cellular acidosis

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47
Q

Proliferation Phase (days 3-20)

A
  • Second phase
  • involves both epithelial cells and CT
  • Purpose is to cover the wound and impart strength to injured area
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48
Q

Proliferation phase characteristics

A
  • Removal of noxious stimuli
  • Growth of capillary beds into area
  • collagen formation
  • granulation tissue formation
  • very fragile
  • easily injured tissue
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49
Q

Proliferation clinical signs

A
  • decreasing edema
  • pain felt with tissue resistance
  • Tender to palpation but less than when acute
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50
Q

Proliferation Phase impairments

A
  • Pain at end ROM
  • decreasing soft tissue edema
  • decreasing joint effusion
  • developing soft tissue, muscle, & joint contractures
  • developing muscle weakness
  • decreased functional use of the part or associated areas
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51
Q

Epithelialization

A
  • Provides protective barrier to seal wound
  • uninjured epithelial>migrate over injured area> cover wound surface> close defect
  • stimulus> loss of contact inhabition
  • stop when migrating cells come in contact with other cells (contact inhabition)
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52
Q

Collagen Production

A
  • Fibroblasts produce collagen
  • Fibroblast growth occurs in CT (fibroplasia)
  • Fibroblasts> procollagen> tropocollagen> collagen fibrils> collagen filaments> collagen fibers
  • granulation tissue
  • infection, edema, excessive stress can cause additional inflammation and collagen production> can limit function
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53
Q

granulation tissue

A

composed of capillaries, fibroblasts, and myofibroblasts

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54
Q

Initially what type of collagen is formed?

A

Type III collagen

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55
Q

What do collagen cross links do?

A

Allow for increased tensile strength

  • allow early, controlled movement
  • proper growth and alignment develops if tensile loaded in the line of normal stress to that tissue
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56
Q

By day 12 of collagen production…

A

type III collagen starts being replaced by more mature and stronger type I collagen
-Amt of collagen in wound and tensile strength linearly related to O2 available to healing tissue

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57
Q

Wound contraction

A
  • Final mechanism for tissue repair
  • pulls edges of wound together
  • begins approx 5 days post injury
  • myofibroblasts> pull epithelial layer inward
  • rate proportional to # of myofibroblasts
  • if uncontrolled can lead to contractures
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58
Q

Wound closure: muscle and skin

A

5-8 days

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59
Q

Wound closure: tendon and ligament

A

3-6 weeks

60
Q

Neovascularization

A
  • Angiogenesis > growth of new blood vessels

- immobilization helps protect new vessels and prevents microhemorrhaging

61
Q

Maturation phase (day 9 and on)

A
  • Longest phase; can last over a year
  • changes occur in size, form, and strength of scar
  • goal: restore prior function of injured tissue
62
Q

Maturation phase characteristics

A
  • Maturation of CT
  • Contracture of scar tissue
  • remodeling of scar
  • collagen aligns to stress
63
Q

Maturation phase clinical signs

A
  • absence of inflammation
  • pain after tissue resistance
  • no longer TTP
64
Q

Maturation phase impairments

A
  • Soft tissue contractures
  • limited AROM/PROM/Joint play
  • decreased muscle performance
  • decreased functional use of part
  • inability to function normally
  • impairments due to scar tissue
65
Q

Maturation phase: syntheis/lysis

A
  • Synthesis and lysis can last 12-24 months

- if synthesis dominates over lysis-hypertrophic or keloid scar can result

66
Q

Maturation phase: scars

A
  • if scar tissue remains redder than sourrounding tissue remodeling is still occuring
    • loss of mobility can be reversed
  • scars are inelastic, mobility occurs due to multiple folds in scar tissue
67
Q

Maturation phase: induction theory

A
  • Scar attempts to mimic characteristics of injured tissue
  • dense tissue types have preference when multiple tissue types are close together
    • repaired tendon immobilized over bone fracture may
      result
68
Q

Maturation phase: tension theory

A
  • internal & external stresses applied during maturation phase determine final tissue structure
  • Madden and Arem- successful remodeling: phases of repair process in which mechanical processes were introduced and the nature of applied forces
  • tension during healing > increased tensile strength
69
Q

Chronic Inflammation

A

Simultaneous progression of active inflammation. Tissue destruction & healing

  • months to years
  • occurs due to inflammatory process being unable to rid that area of the cause of injury and restore function
70
Q

Chronic inflammation arises by:

A

Persistence of the injurious agent
- EX. Cumulative truama
Some interference with the normal healing process
- EX. immune response to an altered host tissue or foreign material

71
Q

Chronic inflammation cellular response

A

Macrophage, lymphocytes, & plasma cells concentrate in the area of injury

  • release chemical mediators that are chemotactic to other macrophages
  • results in less stress being needed to continue the process
  • increased fibroblast proliferation
    • increased collagen production ( scar/adhesion)
    • increased loss of function
72
Q

Recurring inflammation

A
  • Restarting the acute process before previous episode has finished
  • Takes less trauma to begin inflammatory response
  • Can be caused by overly aggressive rehab or too soon return to function
73
Q

Regeneration healing mechanism

A

Restoration of tissue that is identical to injured tissue

74
Q

Repair healing mechanism

A
  • Fibrous scar formation

- Structural & functional properties of injured tissue altered

75
Q

Combined healing mechanism

A

-Soft tissue healing, in most cases, through a combination or regeneration and repair

76
Q

Ideal healing

A

injured tissue> back to normal

77
Q

acceptable healing

A

Partial restoration of identical tissue > can function moderately well

78
Q

minimal healing

A

Structural integrity= will have reoccurance

79
Q

Failed healing

A

No chance of functional integrity

80
Q

Skin healing: hemostasis

A
  • Bleeding > blood clotting cascade > coagulation > release of pro-inflammatory molecules
  • Fibrin clot provides early cellular matrix for inflammatory phase
81
Q

Skin healing: inflammation

A
  • Inflammatory cells enter site
  • phagocytosis of necrotic tissue
  • Release of growth factors
    • stimulate/regulate function of migrating cells
  • Prepares wound for proliferation stage
82
Q

Skin healing: Proliferation

A
  • Repair tissue placed into the wound
  • Fibroblasts migrate to the area and proliferate (fibroplasia)
  • granulation buds develop (angiogensis)
  • new collagen fills wound
    • weak & disorganized
83
Q

Skin healing: maturation

A
  • Collagen matures from type III to type I
  • Collagen remodeled based upon stresses applied
  • Normal orientation of fibers develops
84
Q

Skin healing: outcome of repair tissue

A

Repair tissue:

  • weaker and less elastic than original
  • structural, biomechanical & functional properties often match that of original skin
85
Q

Skin healing: quality of healing

A

Acceptable to ideal

86
Q

Tendon healing: hemostasis

A
  • Bleeding > blood clotting cascade > release of pro-inflammatory molecules
  • Fibin clot provides early cellular matrix for inflammatory phase
87
Q

Tendon healing: inflammation

A
  • Inflammatory cells enter site
  • Phagocytosis of necrotic tissue
  • Tenocytes migrate to site of injury
  • type III collagen synthesis is started
88
Q

Tendon healing: proliferation

A
  • Repair tissue placed into the wound
  • Fibroblasts migrate to area and prolifeate
  • Granulation tissue develops
  • capillary buds develop
  • New collagen type III fills wound
    • weak and disorganized
89
Q

Tendon healing: maturation

A
  • Collagen matures from type III to type I
  • tenocytes and collagen remodeled based upon stresses applied
  • immature fibrous tissue develops into scar-like tendon tissue
90
Q

Tendon healing: outcome of repair tissue

A
  • Weaker and less elastic than original but functional

- structural, biomechanical, and functional properties never match original tendon

91
Q

Tendon healing: quality of healing

A

Minimal to acceptable

92
Q

Ligament healing: hemostasis

A
  • Disrupted ends of ligament retract

- bleeding > blood clotting cascade > coagulation > release of pro-inflammatory molecules

93
Q

Ligament healing: inflammation

A
  • Increased vascularity and flow of blood fills in gap between ends of disrupted ligament
  • inflammatory cells enter site
  • phagocytosis of necrotic tissue
94
Q

Ligament healing: proliferation

A
  • Granulation tissue develops
  • capillary buds develop
  • scar tissue develops by hypertrophic fibroblast cells
  • scar becomes less disorganized with fibers aligning along lines of stress
  • collagen content abnormal ( more type III, than type I, more type V than normal)
95
Q

Ligament healing: maturation

A
  • Scar tissue becomes more like ligament tissue

- structure, composition, function not the same as original ligament tissue

96
Q

ligament healing: outcome of repair tissue

A
  • weaker, less elastic than original but functional

- structural, biomechanical, and functional properties never match original ligament

97
Q

Ligament healing: quality of repair

A

minimal to acceptable

98
Q

Articular cartilage healing grade I: hemostasis

A
  • Chondrocyte necrosis with no hemorrhage response
  • no hemostasis
  • Doesn’t bleed
  • NO inflammation, proliferation
99
Q

Articular cartilage healing grade I: maturation

A
  • Repair response insufficient to maintain normal articular surface
  • limited ability of chondrocytes to restore lost matrix
  • loss of compressive and tensile stiffness properties of cartilage
  • irreversible articular degeneration
100
Q

Articular cartilage healing grade I: outcome of repair tissue

A

Absent

101
Q

Articular cartilage healing grade I: quality of healing

A

Failed

102
Q

Articular cartilage healing grade II: Hemostasis

A
  • Chondrocyte necrosis with no hemorrhage response
  • NO hemostasis
  • no inflammation or proliferation
103
Q

Articular cartilage healing grade II: maturation

A
  • Metabolic and mitotic activity of remaining chondrocytes limited in area surrounding defect or injury site
  • new matrix remains on periphery and does not fill defect
104
Q

Articular cartilage healing grade II: outcome of repair tissue

A

absent

105
Q

Articular cartilage healing grade II: quality of healing

A

Failed

106
Q

Articular cartilage healing grade III: hemostasis

A
  • Enough damage to initiate inflammatory response as with other vascularized tissue
  • bleeding > blood clotting cascade > coagulation > release of pro-inflammatory molecules
  • involves bony interface
107
Q

Articular cartilage healing grade III: inflammation

A

Recruitment and proliferation of chondrocyte-like cells begins

108
Q

Articular cartilage healing grade III: Proliferation

A
  • Chondrocyte-like cells differentiate into chondroblasts, chondrocytes, and osteoblasts
  • cartilage and matrix synthesis begins
  • limited capillary budding (angiogenesis)
109
Q

Articular cartilage healing grade III: maturation

A
  • Osteochondral occification heals bone defect (months)
  • fissuring of articular surfaces occurs over time
  • Degenerative changes occur
110
Q

Articular cartilage healing grade III: outcome of repair tissue

A
  • Matrix of hyalin and fibrocartilage tissue at wound site

- Repair cartilage does not approximate structure or function of intace articular cartilage

111
Q

Articular cartilage healing grade III: quality of healing

A

-minimal to failed

112
Q

Skeletal muscle healing: hemostais

A
  • Bleeding > blood clotting cascade > coagulation > release of pro-inflammatory molecules
  • Fibrin clot provides early cellular matrix for inflammatory phase
113
Q

Skeletal muscle healing: inflammation

A
  • inflammatory cells enter the site
  • phagocytosis of necrotic tissue
  • myofibers rupture and become necrotic
  • Sarcoplasmic membrane ruptures
  • contraction band seals off defect
  • angiogensis
  • Satellite cells begin formation of new myofibers
114
Q

Skeletal muscle healing: Proliferation/maturation regeneration of disrupted myofibers

A
  • Satellite cells > Proliferate > differentiate into myoblasts > form myotubes
  • myotubes fuse with myofibers
  • good vascularization and regeneration of inramuscular nerve necessary
115
Q

Skeletal muscle healing: Proliferation/maturation Formation of CT scar

A
  • Fibrin and fibroblasts fill gap between myofibers with CT forming functionally disabling scar
  • large proportion of skeletal muscle lesions heal without forming this scar
116
Q

Skeletal muscle healing: outcome of repair tissue

A
  • Mixture of regenerative and repair muscle fibers

- Partial to normal functional ability

117
Q

Skeletal muscle healing: Quality of healing

A

Acceptable to ideal

118
Q

Bone healing: Hemostasis

A
  • Bleeding at injury site

- hematoma formation to control bleeding

119
Q

Bone healing: inflammation

A
  • Osteogenic cells and granulation tissue develops

- Provides an environment for collagen synthesis and osteogenesis

120
Q

Bone healing: Proliferation

A
  • Angiogenesis
  • Fibrocartilaginous callus forms
  • Bone matrix develops
  • mineralization of bone matrix
121
Q

Bone healing: Maturation

A
  • Fracture site becomes stable
  • osteoclastic activity resorbs existing bone
  • osteoblastic activity lays down new bone
  • Fractured bone resumes normal structure, size, shape
122
Q

Bone healing: outcome of repair tissue

A

Identical to original bone

123
Q

Bone healing: quality of healing

A

ideal

124
Q

Local identify factors that can affect tissue healing

A
  • Type, size, location of injury
  • infection
  • vascular supply
  • external forces
  • movement
  • early movement may delay healing
  • early passive movement (CPM) may improve function
125
Q

Systemic identify factors that can affect tissue healing

A
  • Age
  • Disease
  • Medications
  • Nutrition
126
Q

Physical agent response: Initial acute injury phase

A

Identified by the 5 cardinal signs of inflammation

  • Attempt to limit swelling & pain
  • cryotherapy (PRICE)
  • compression
  • Electrical Stimulation (HVPG)
  • Ultrasound (pulsed, low intensity)
  • Low-power laser
127
Q

Inflammatory stage care stages

A
  • immediate care: 0-12 hours
  • Transition care: 12 hrs to 4 days
  • Subacute care: 4 days to 14 days
  • Postacute care: after 14 days
128
Q

Immediate care

A

Price or rices

  • protect
  • rest
  • ice
  • compression
  • elevation
129
Q

Immediate care decreases or minimizes development of:

A
  • Swelling
  • Pain
  • Muscle spasm
  • neural inhibition
  • secondary injury
  • therefore total injury
130
Q

Immediate care: ice

A

Limits secondary injury

  • decreased blood flow theory
  • Decreased secondary injury theory
  • metabolic- oxygen debt due to ischemia > ice decreases metabolism
  • chemical- ice limits permeability thus leakage of protein rich fluid into tissue
131
Q

Immediate care: compression

A
  • increases external capillary pressure
  • Decreases CFP
  • Decreases edema formation
132
Q

Immediate care: elevation

A

decreases capillary hydrostatic pressure

133
Q

immediate care: protect/stabalize

A
  • Allows muscles to relax

- reduces pain and neural inhibition

134
Q

Transition care: management guidelines

A 
pt education
- duration of phase
- precautions
-contraindications
Protection of injured part
- PRICE
- control pain, edema, spasm
135
Q

Transition care: prevention of adverse effects of immobilization

A
  • PROM: within limit of pain
  • low dose grade I or II non-thrust manipulations
  • muscle setting sub maximal isometrics
  • massage
  • associated areas:
    • ROM
    • muscle strength
    • functional activites
    • circulation
136
Q

Transition care: physical agent response

A
  • Swelling subsiding but area still painful and warm to touch
  • Goal: limit pain & swelling
    • cryotherapy (PRICE)
    • compression
    • Electrical stim (HVPG)
    • Ultrasound (pulsed, low intensity)
    • low-power laser
137
Q

Proliferation phase: management guidlines

A 
pt education
- duration of phase
-precautions/contraindications
-signs of pushing too hard
Management of pain and inflammation
initiate ACTIVE exercises
- multi angle sub max isometrics
- AROM
-endurance
- protected closed chain exercise
138
Q

Proliferation phase: initiation & progression to stretching

A
  • Warm the tissues
  • inhibition techniques
  • Grade III or IV non thrust mobilization
  • stretching
  • massage
  • encourage pt to use new ROM
  • correct predisposing factors
139
Q

Proliferation phase: physical agent response

A
  • swelling stopped and pain subsiding
  • consider switching from cold to heat
  • intermittent compression
  • electrical stimulation (NMES,TENS)
    • muscle contraction now acceptable
140
Q

Maturation phase: management guidelines

A 
pt education
- pt must take charge of self rehab
- instruct in signs of excessive stress on tissues
Progress exercises
- sub max to maximal
- activity specific
- single plane to multi plane
-proper biomechanics
141
Q

Maturation phase: goals

A
  • Progress stretching ( tissue specific)
  • progress muscle performance exercises
  • Progress to high demand activities
142
Q

Maturation phase: physical agents response

A
  • goal: attempt to realign collagen fibers according to tensile stresses and strains
  • most phys agents may be safely used
    • deep heat ( continuous US, Diathermy)
    • low-power laser
    • electrical stimulation
143
Q

Physical agents that stimulate the healing process

A
  • Ultrasound
  • Electrical stimulation
  • MHP
144
Q

Physical agents that promote lymphatic drainage to hasten repair process

A
  • Massages
  • cryokinetics
  • compression devices
145
Q

Physical agents that modulate pain to allow for therapy exercises

A
  • Cryokinetics
  • Cryostretch
  • TENS

Physical Agents (21 decks)

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