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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
Capillary filtration Pressure equation
CFP= (CHP + TOP) - (THP + COP)
26
CHP
Capillary hydrostatic pressure
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TOP
Tissue osmotic pressure
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THP
Tissue hydrostatic pressure
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COP
Capillary osmotic pressure
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hydrostatic pressure
pressure exerted by a column of water (pushes water)
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osmotic pressure
pressure resulting from attraction of fluid by free proteins (pulls water)
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Changes in Capillary filtration pressure (CFP) after injury
- TOP increases - Pulls fluid into tissues - edema and swelling results - but initial swelling after injury from hemorrhaging
33
Erythrocyte response to injury- inflammatory stage
play minor role in inflammatory process
34
Leukocyte response to injury- inflammatory stage
- clear injured area of debris and microorganisms | - set the stage for tissue repair
35
Cellular response: first 24 hours
Polymorphonuclear leukocytes - Neutrophils - Basophils - Eosinophils
36
Neutrophils
- pagocytosis | - release enzymes (protease) & collagenolytic enzymes (collagenases)
37
Basophils
- release histamine - contribute to increased vascular permeability - apply cold= decrease amt of histamine= vasoconstriction
38
Eosinophils
Phagocytosis
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Cellular response: first 24-48 hrs
Mononuclear leukocytes - Monocytes - Lymphocytes
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Monocytes
- converted into macrophages - collagenase - fibronectin - hydrogen peroxide, ascorbic acid, lactic acid - Most effective in oxygen rich environment in tissue
41
Lymphocytes
Supply antibodies | - mediate immune response
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Immune response to injury
- B lymphocytes - T lymphocytes - Activation of complement system
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immune response: B lymphocytes
release antibodies into bloodstream
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immune response: T lymphocytes
Assist B cells in regulation of cloning
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immune response: activation of complement system
Series of enzymatic plasma proteins - increased vascular permeability - stimulate phagocytosis - act as chemotactic stimuli for leukocytes
46
Metabolic response to injury
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> >> increased cellular H20> cell swells> burst or die - increased cellular acidosis
47
Proliferation Phase (days 3-20)
- Second phase - involves both epithelial cells and CT - Purpose is to cover the wound and impart strength to injured area
48
Proliferation phase characteristics
- Removal of noxious stimuli - Growth of capillary beds into area - collagen formation - granulation tissue formation - very fragile - easily injured tissue
49
Proliferation clinical signs
- decreasing edema - pain felt with tissue resistance - Tender to palpation but less than when acute
50
Proliferation Phase impairments
- 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
51
Epithelialization
- 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)
52
Collagen Production
- 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
53
granulation tissue
composed of capillaries, fibroblasts, and myofibroblasts
54
Initially what type of collagen is formed?
Type III collagen
55
What do collagen cross links do?
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
56
By day 12 of collagen production...
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
57
Wound contraction
- 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
58
Wound closure: muscle and skin
5-8 days
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Wound closure: tendon and ligament
3-6 weeks
60
Neovascularization
- Angiogenesis > growth of new blood vessels | - immobilization helps protect new vessels and prevents microhemorrhaging
61
Maturation phase (day 9 and on)
- Longest phase; can last over a year - changes occur in size, form, and strength of scar - goal: restore prior function of injured tissue
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Maturation phase characteristics
- Maturation of CT - Contracture of scar tissue - remodeling of scar - collagen aligns to stress
63
Maturation phase clinical signs
- absence of inflammation - pain after tissue resistance - no longer TTP
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Maturation phase impairments
- 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
Maturation phase: syntheis/lysis
- Synthesis and lysis can last 12-24 months | - if synthesis dominates over lysis-hypertrophic or keloid scar can result
66
Maturation phase: scars
- 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
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Maturation phase: induction theory
- 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
Maturation phase: tension theory
- 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
Chronic Inflammation
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
Chronic inflammation arises by:
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
Chronic inflammation cellular response
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
Recurring inflammation
- 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
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Regeneration healing mechanism
Restoration of tissue that is identical to injured tissue
74
Repair healing mechanism
- Fibrous scar formation | - Structural & functional properties of injured tissue altered
75
Combined healing mechanism
-Soft tissue healing, in most cases, through a combination or regeneration and repair
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Ideal healing
injured tissue> back to normal
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acceptable healing
Partial restoration of identical tissue > can function moderately well
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minimal healing
Structural integrity= will have reoccurance
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Failed healing
No chance of functional integrity
80
Skin healing: hemostasis
- Bleeding > blood clotting cascade > coagulation > release of pro-inflammatory molecules - Fibrin clot provides early cellular matrix for inflammatory phase
81
Skin healing: inflammation
- Inflammatory cells enter site - phagocytosis of necrotic tissue - Release of growth factors * stimulate/regulate function of migrating cells - Prepares wound for proliferation stage
82
Skin healing: Proliferation
- Repair tissue placed into the wound - Fibroblasts migrate to the area and proliferate (fibroplasia) - granulation buds develop (angiogensis) - new collagen fills wound * weak & disorganized
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Skin healing: maturation
- Collagen matures from type III to type I - Collagen remodeled based upon stresses applied - Normal orientation of fibers develops
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Skin healing: outcome of repair tissue
Repair tissue: - weaker and less elastic than original - structural, biomechanical & functional properties often match that of original skin
85
Skin healing: quality of healing
Acceptable to ideal
86
Tendon healing: hemostasis
- Bleeding > blood clotting cascade > release of pro-inflammatory molecules - Fibin clot provides early cellular matrix for inflammatory phase
87
Tendon healing: inflammation
- Inflammatory cells enter site - Phagocytosis of necrotic tissue - Tenocytes migrate to site of injury - type III collagen synthesis is started
88
Tendon healing: proliferation
- 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
Tendon healing: maturation
- 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
Tendon healing: outcome of repair tissue
- Weaker and less elastic than original but functional | - structural, biomechanical, and functional properties never match original tendon
91
Tendon healing: quality of healing
Minimal to acceptable
92
Ligament healing: hemostasis
- Disrupted ends of ligament retract | - bleeding > blood clotting cascade > coagulation > release of pro-inflammatory molecules
93
Ligament healing: inflammation
- Increased vascularity and flow of blood fills in gap between ends of disrupted ligament - inflammatory cells enter site - phagocytosis of necrotic tissue
94
Ligament healing: proliferation
- 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)
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Ligament healing: maturation
- Scar tissue becomes more like ligament tissue | - structure, composition, function not the same as original ligament tissue
96
ligament healing: outcome of repair tissue
- weaker, less elastic than original but functional | - structural, biomechanical, and functional properties never match original ligament
97
Ligament healing: quality of repair
minimal to acceptable
98
Articular cartilage healing grade I: hemostasis
- Chondrocyte necrosis with no hemorrhage response - no hemostasis - Doesn't bleed - NO inflammation, proliferation
99
Articular cartilage healing grade I: maturation
- 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
Articular cartilage healing grade I: outcome of repair tissue
Absent
101
Articular cartilage healing grade I: quality of healing
Failed
102
Articular cartilage healing grade II: Hemostasis
- Chondrocyte necrosis with no hemorrhage response - NO hemostasis - no inflammation or proliferation
103
Articular cartilage healing grade II: maturation
- 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
Articular cartilage healing grade II: outcome of repair tissue
absent
105
Articular cartilage healing grade II: quality of healing
Failed
106
Articular cartilage healing grade III: hemostasis
- 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
Articular cartilage healing grade III: inflammation
Recruitment and proliferation of chondrocyte-like cells begins
108
Articular cartilage healing grade III: Proliferation
- Chondrocyte-like cells differentiate into chondroblasts, chondrocytes, and osteoblasts - cartilage and matrix synthesis begins - limited capillary budding (angiogenesis)
109
Articular cartilage healing grade III: maturation
- Osteochondral occification heals bone defect (months) - fissuring of articular surfaces occurs over time - Degenerative changes occur
110
Articular cartilage healing grade III: outcome of repair tissue
- Matrix of hyalin and fibrocartilage tissue at wound site | - Repair cartilage does not approximate structure or function of intace articular cartilage
111
Articular cartilage healing grade III: quality of healing
-minimal to failed
112
Skeletal muscle healing: hemostais
- Bleeding > blood clotting cascade > coagulation > release of pro-inflammatory molecules - Fibrin clot provides early cellular matrix for inflammatory phase
113
Skeletal muscle healing: inflammation
- 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
Skeletal muscle healing: Proliferation/maturation regeneration of disrupted myofibers
- Satellite cells > Proliferate > differentiate into myoblasts > form myotubes - myotubes fuse with myofibers - good vascularization and regeneration of inramuscular nerve necessary
115
Skeletal muscle healing: Proliferation/maturation Formation of CT scar
- 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
Skeletal muscle healing: outcome of repair tissue
- Mixture of regenerative and repair muscle fibers | - Partial to normal functional ability
117
Skeletal muscle healing: Quality of healing
Acceptable to ideal
118
Bone healing: Hemostasis
- Bleeding at injury site | - hematoma formation to control bleeding
119
Bone healing: inflammation
- Osteogenic cells and granulation tissue develops | - Provides an environment for collagen synthesis and osteogenesis
120
Bone healing: Proliferation
- Angiogenesis - Fibrocartilaginous callus forms - Bone matrix develops - mineralization of bone matrix
121
Bone healing: Maturation
- Fracture site becomes stable - osteoclastic activity resorbs existing bone - osteoblastic activity lays down new bone - Fractured bone resumes normal structure, size, shape
122
Bone healing: outcome of repair tissue
Identical to original bone
123
Bone healing: quality of healing
ideal
124
Local identify factors that can affect tissue healing
- Type, size, location of injury - infection - vascular supply - external forces - movement * early movement may delay healing * early passive movement (CPM) may improve function
125
Systemic identify factors that can affect tissue healing
- Age - Disease - Medications - Nutrition
126
Physical agent response: Initial acute injury phase
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
Inflammatory stage care stages
- 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
Immediate care
Price or rices - protect - rest - ice - compression - elevation
129
Immediate care decreases or minimizes development of:
- Swelling - Pain - Muscle spasm - neural inhibition - secondary injury - therefore total injury
130
Immediate care: ice
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
Immediate care: compression
- increases external capillary pressure - Decreases CFP - Decreases edema formation
132
Immediate care: elevation
decreases capillary hydrostatic pressure
133
immediate care: protect/stabalize
- Allows muscles to relax | - reduces pain and neural inhibition
134
Transition care: management guidelines
``` pt education - duration of phase - precautions -contraindications Protection of injured part - PRICE - control pain, edema, spasm ```
135
Transition care: prevention of adverse effects of immobilization
- 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
Transition care: physical agent response
- 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
Proliferation phase: management guidlines
``` 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
Proliferation phase: initiation & progression to stretching
- Warm the tissues - inhibition techniques - Grade III or IV non thrust mobilization - stretching - massage - encourage pt to use new ROM - correct predisposing factors
139
Proliferation phase: physical agent response
- swelling stopped and pain subsiding - consider switching from cold to heat - intermittent compression - electrical stimulation (NMES,TENS) * muscle contraction now acceptable
140
Maturation phase: management guidelines
``` 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
Maturation phase: goals
- Progress stretching ( tissue specific) - progress muscle performance exercises - Progress to high demand activities
142
Maturation phase: physical agents response
- 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
Physical agents that stimulate the healing process
- Ultrasound - Electrical stimulation - MHP
144
Physical agents that promote lymphatic drainage to hasten repair process
- Massages - cryokinetics - compression devices
145
Physical agents that modulate pain to allow for therapy exercises
- Cryokinetics - Cryostretch - TENS

Physical Agents (21 decks)

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