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KIN 440 > Tissue Repair > Flashcards

Tissue Repair Flashcards

1
Q

Mechanisms and characteristics of MSK trauma:

A
  • mechanical forces

- tissue susceptibility to trauma

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2
Q

Mechanical forces:

A
  • tissues can resist a particular load

- forces acting on the body

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3
Q

Tissue susceptibility to trauma:

A
  • viscoelastic properties
  • deformation = yield point
  • mechanical failure
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4
Q

Stress-strain curve:

A
  • y axis = stress or load/unit area
  • x axis = strain or deformation/original length
  • zone 1 = elastic properties
  • zone 2 = plastic changes
  • point 1 = yield point
  • end point = tissue failure (injury)
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5
Q

Macrotraumatic injuries:

A
  • acute MOI: able to articulate how injured and why
  • known DOI: onset short period of time
  • S&S: may produce levels of immediate pain and functional disability
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6
Q

Examples of macrotraumatic injuries:

A
  • fractures
  • dislocations
  • contusion
  • sprains
  • strains
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7
Q

Microtraumatic injuries:

A
  • chronic MOI: may not be able to articulate how or why injured
  • insidious DOI: onset long period of time from repetitive overload, incorrect mechanics, previous injury
  • S&S: may be painful but typically able to function
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8
Q

Examples of microtraumatic injuries:

A
  • tendinitis
  • tenosynovitis
  • bursitis
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9
Q

Secondary systemic complications:

A
  • the response to the primary injury
  • inflammatory response to focal area occurs over time (seconds or minutes to hours or days)
  • secondary tissue response
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10
Q

Secondary injury: inflammatory response to focal area includes:

A
  • cellular injury mechanism results in edema (swelling), hemorrhage (bruising, redness, warmth)
  • impaired metabolism to tissues leads to ischemia (inadequate blood supply to healthy tissues). Results in hypoxic response to surrounding tissues
  • creates oxidative stress (toxic tissue) leads to cell death
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11
Q

Secondary tissue response:

A
  • further tissue trauma

- possibly infection

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12
Q

Secondary tissue response may result in:

A
  • muscular spasm
  • extremity guarding
  • more swelling
  • more bruising
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13
Q

Plan for rehabilitation programming must be built upon the framework for ____ ____.

A

tissue repair

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14
Q

Tissue repair:

A

restoration of tissue and of function after an injury

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15
Q

2 processes of tissue repair:

A
  • regeneration

- replacement

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16
Q

Regeneration (tissue repair):

A

healing in which new growth completely restores portions of damaged tissue to their normal state

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17
Q

Replacement (tissue repair):

A

healing in which severely damaged or non-regenerable tissues are repaired by scarring

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18
Q

Phases of tissue repair are ______ phases.

A

non-definitive

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19
Q

Types of responses in each phase:

A
  • vascular
  • cellular
  • chemical
  • clinical
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20
Q

Phases of tissue response to injury:

A
  • inflammatory response phase
  • fibroblastic repair phase
  • maturation-remodeling phase
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21
Q

Clinical responses to tissue injury:

A
  • altered cellular metabolism and chemical mediators

- macroscopic characteristics of an inflammatory response

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22
Q

Macroscopic characteristics of an inflammatory response includes:

A
  • swelling
  • heat
  • altered function
  • redness
  • pain: tenderness, point tenderness
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23
Q

Plan for clinical responses to tissue injury:

A

initial management and treatment response is critical in the repair and healing process

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24
Q

Acute inflammation:

A
  • short onset and duration (weeks)
  • begins immediately following damage to tissue (MOI)
  • change in hemodynamics (blood system), production of exudate (swelling) and leukocytes (garbage collector)
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25
Q

Chronic inflammation:

A
  • insidious onset, or has been long duration of time (chronic)
  • occurs when the acute inflammation response fails as may be in a state of repeated damage to tissue (months to years)
  • as not restored to a normal physiological state, there is a proliferation of extensive scar tissue
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26
Q

Proliferation of extensive scar tissue includes:

A
  • chronic change in hemodynamics (injuring agents are not eliminated)
  • repeated production of connective tissue and tissue degeneration, production and presence of garbage collectors including macrophages, lymphocytes (different chemical mediators)
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27
Q

Phase 1 inflammatory response:

A
  • initial reaction to tissue damage (injury)
  • occurring immediately (post injury) from time of injury (0 to 4-7 days)
  • injury can be caused by trauma, chemical agents, thermal extremes, pathogenic organisms
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28
Q

External injury results in …

A

tissue death

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29
Q

Internal injury results in …

A

tissue (cellular) death

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30
Q

How does internal injury result in tissue (cellular) death?

A
  • decreased oxygen to area increases cell death by secondary hypoxic injury
  • phagocytosis (garbage collectors) will add to cell death due to excess digestive enzymes
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31
Q

In phase 1, goals of a plan may include:

A
  • protect
  • localize (secondary injury)
  • decrease injurious agents
  • prepare for healing and tissue repair
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32
Q

Management in phase 1:

A
  • critical to limiting cell death
  • Protect, Rest, Optimal loading, Ice, Compression, Elevation are critical to limiting cell death
  • RICE –> PRICE –> POLICE
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33
Q

Vascular response:

A
  • blood vessels vasoconstrict (serotonin)
  • then blood vessels vasodilate (histamine, heparin)
  • increase blood flow and permeability results in swelling
  • controlled by chemical response, prepares the tissue for cellular response
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34
Q

Cellular response:

A
  • mast cells are released in cell damage (heparin, histamine, serotonin)
  • phagocytocis
  • leukocytes (leukotaxin)
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35
Q

Phagocytocis:

A

damaged tissue encourages leukocytes to enter tissue and clear away all damage (phagocytic activity)

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36
Q

Leukocytes (leukotaxin):

A

allows for cell margination = increase cell permeability for WBC to flow thru cell walls forming exudate

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37
Q

Chemical mediators such as … are released to facilitate healing:

A
  • histamine
  • serotonin
  • bradykinin
  • heparin
  • prostaglandins
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38
Q

Research in chemical response suggests that decrease mediators =

A
  • decrease inflammation

- healing needs to progress through the healing process

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39
Q

Example of inflammatory response:

A
  1. injury to cell
  2. chemical mediators liberated (histamine, leukotrienes, cytokines)
  3. vascular reaction (vasoconstriction –> vasodilation –> exudate creates stasis)
  4. platelets and leukocytes adhere to vascular wall
  5. phagocytosis
  6. clot formation
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40
Q

Phase 2 =

A

fibroblastic repair phase

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41
Q

In phase 2, _____ and _____ activity occurs resulting in ____ ____ –> ______.

A
  • proliferative
  • regenerative
  • scar formation
  • fibroplasia
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42
Q

Phase 2 has 3 phases:

A
  • resolution
  • restoration
  • regeneration
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43
Q

Phase 2 time frame:

A
  • 48 hours to 6 weeks following DOI

- depends on many factors

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44
Q

Phase 2 time frame depends on:

A
  • tissue damage (debris)
  • type of tissue (revascularization)
  • nutrition (vitamin C)
  • health of client
  • re-injury
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45
Q

What happens during phase 2?

A
  • cleaning of fibrin clot and cellular debris (erythrocytes)
  • restore tissue formation of a scar
  • regenerates or replacement of tissue by same tissue (increase blood flow delivery (aerobic) for nutrient delivery as capillary buds develop)
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46
Q

Phase 2 does not progress until…

A

swelling (S&S) of acute inflammatory phase begin to subside

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47
Q

How does scar formation work?

A
  • granulation tissue (fibroblasts, collagen) develops with breakdown of fibrin clot
  • firm, inelastic mass (no capillary circulation yet)
  • develops from exudate with high protein and debris level resulting in granulation tissue
  • invaded by fibroblasts and collagen deposited randomly forming a dense scar (require 3-14 weeks, may require 6 months for increased scar tensile strength)
48
Q

Tissue examples of scar formation:

A
  • ligaments

- muscles

49
Q

Phase 3 =

A

maturation-remodelling phase

50
Q

Phase 3 overlaps with….

A

previous phase of regeneration phase

51
Q

Phase 3 consists of _____ of ____ over time.

A
  • realignment

- collagen

52
Q

Phase 3 time frame:

A
  • may require several years to complete (maturation)

- depends on the amount and type of scar/tissue

53
Q

First 3-6 weeks of phase 3 involves laying down of ____ and strengthening of _____.

A
  • collagen

- fibres

54
Q

At ~3 weeks in phase 3:

A

firm, strong, contracted nonvascular scar

55
Q

At ~3 months to 2 years in phase 3:

A
  • enhanced scar tissue strength (remodelling) with ongoing and continued breakdown and synthesis of collagen
  • increased stress and strain results in increased collagen realignment
  • balance must be maintained between synthesis and lysis
56
Q

How do we consider forces applied in rehab in phase 3?

A
  • balance between immobilization and mobilization time frames relative to tissue repair timelines
  • role of mobilization
57
Q

Wolff’s Law:

A
  • bone will adapt to the loads under which it is placed

- muscle will respond to forces (physical demands) placed upon it

58
Q

Initial _____ may be necessary for initiating healing.

A

immobilization

59
Q

Controlled mobilization into repair phase enhances:

A
  • scar formulation (remodelling)
  • revascularization
  • muscle regeneration
  • fibre reorientation (alignment)
  • tensile properties
60
Q

Controlled stability in activity allows for…

A

gradual return to normal levels of function

61
Q

Epithelial (skin) healing:

A

full healing capacity through repair phases of healing, scar, stitch for approximation of tissue

62
Q

Cartilage (meniscus, labrum) healing:

A

healing is limited to slow, poor blood supply, no healing in defective tissue

63
Q

Ligament healing:

A
  • full healing capacity through repair phases
  • 3 degrees extent of injury
  • may require surgical repair in complete tears (grade 3)
64
Q

Skeletal muscle healing:

A
  • full healing capacity through repair phases
  • may result in functional scar tissue
  • 3 degrees extent of injury
  • may require surgery in complete tears pending approximation
65
Q

Nerve healing:

A
  • peripheral nerve regeneration properties of 3 mm/day

- CNS regenerates poorly

66
Q

Bone healing:

A
  • full healing capacity
  • complex healing (bone repair phases)
  • new bone in remodelling phase
67
Q

____ ____ and _____ are necessary for repair. Certain organic _____ (____ conditions) may sow or inhibit the healing process; poor vascular supply.

A
  • blood supply
  • nutrients
  • disorders (blood conditions)
68
Q

Healing properties due to certain factors may change repair, including:

A
  • past tissue injuries or extent/severity of damage
  • irregular or excessive fibrous scar at injury site
  • amount of swelling (edema, hemorrhage)
  • separation of tissue
69
Q

Other factors that can impede or negatively affect healing:

A
  • poor diets (nutrition)
  • health of client
  • muscle spasm or atrophy
  • pain
  • infections
  • age
  • climate and oxygen tension
70
Q

Pain:

A
  • a symptom
  • indicator of injury not of damage
  • pain is individual, pain is subjective
71
Q

Factors involved in pain are a mixture of:

A
  • anatomical structures
  • psychological, social, cultural and cognitive factors
  • physiological reactions
72
Q

Physiological reactions of pain:

A
  • pain receptors: free nerve endings sensitive to extreme mechanical, thermal and chemical energy (ex. skin)
  • pain information transmitted to spinal cord via unmyelinated C fibres and A delta fibres
73
Q

Nervous system is _____ in nature.

A

electrochemical

74
Q

Nociceptive stimuli:

A

body’s processing of harmful stimuli in the nervous system, sensing potential harm

75
Q

Noxious stimuli:

A

an intensity which would result in tissue injury

76
Q

Nociceptive stimuli is a result of….

A

chemical, mechanical or thermal stimulation

77
Q

Stimulated ____ _____ send signal of potential harm Travels along _____ nerves via the ____ ____ to the brain. Frequency of firing determines the _____ of the pain.

A
  • pain receptors
  • afferent
  • spinal cord
  • intensity
78
Q

A delta fibres:

A
  • fast conducting
  • transmits information to the thalamus concerning location of pain and perception of pain being sharp, bright or stabbing
79
Q

C fibres:

A
  • slower conduction
  • transmits info to brain concerning with diffused, dull, aching, throbbing pain
  • signal also passed to limbic cortex providing emotional component to pain
80
Q

Pain sources- types of receptors:

A
  • cutaneous (skin)
  • deep somatic (bone and joints)
  • visceral (body organs)
  • psychogenic
81
Q

Cutaneous pain:

A
  • sharp, bright and burning

- fast and slow onset

82
Q

Deep somatic pain:

A

originates in tendons, muscles, joints, periosteum, and blood vessels

83
Q

Visceral pain:

A

begins in organs and is diffused at first and may become localized

84
Q

Psychogenic pain:

A

felt by the individual but is emotional rather than physical

85
Q

Chronic pain:

A
  • pain continuing beyond average healing timelines

- chronic pain lasts longer than 6 months

86
Q

Referred pain:

A
  • pain occurs away from the site of injury

- may elicit motor or sensory response

87
Q

Types of referred pain:

A
  • myofasial
  • myotome (muscle)
  • dermatome (skin)
  • sclerotome (bone)
88
Q

Myofascial pain:

A
  • trigger points
  • small hyper irritable areas within a muscle resulting in bombardment of CNS
  • can be associated with acute and chronic pain
89
Q

3 ways of describing pain:

A
  • hyperesthesia
  • paresthia
  • anaglesia
90
Q

Pain modulation: mixture of ____ and _____ factors.

A
  • physical

- psychological

91
Q

Pain can be _____ and _____, vary per _____, _____ differences also have an impact.

A
  • subjective
  • psychological
  • individual
  • personality
92
Q

Pain is often worse at ____ due to…

A
  • night

- solitude and absence of external distractions

93
Q

Through ______, we are often able to endure pain and block ______ of minor injuries.

A
  • conditioning

- sensations

94
Q

Gate theory:

A
  • sensory info from cutaneous receptors enters A-beta afferents to dorsal horn of spinal cord
  • pain simultaneously travels along A-delta and c-fibres
  • sensory info overrides pain info, closing gate
  • pain message never received
  • stimulation of large fast nerves can block signal of small pain fibre input
95
Q

Gate control occurs at the level of the ____ _____.

A

spinal cord

96
Q

Gate theory is the rationale for….

A
  • TENS
  • acupressure/puncture
  • thermal agents
  • chemical skill irritants
97
Q

B-endorphins theory:

A
  • stimulation of pain sensory fibres is required
  • neurotransmitters are released by pre-synaptic cells
  • noxious stimuli can trigger release of endorphins (norepinephrine) or serotonin
  • results in activation of pain inhibition transmission, release from hypothalamus (strong analgesic effects, pain modulator)
98
Q

____ ____ is the best reflection of pain and discomfort. Assessment techniques include:

A
  • self report

- OPQRST (OPPQRRRSTTT) questions

99
Q

Other subjective assessments of pain:

A
  • visual analog scales (0-10)
  • pain charts
  • McGill pain questionnaire
  • activity pain indicator profiles
  • numeric rating scale
100
Q

Describe pain based on ___ of pain.

A

history

101
Q

Pain impacts the _____ plan: affects …..

A
  • rehabilitation

- movement or functional movement

102
Q

Pain management:

A
  • use of pain theory

- understand tools

103
Q

Pain management tools for analgesia:

A
  • therapeutic modality: heat/cold
  • therapeutic electrical modality: TENS, acupuncture
  • pharmacological agents (drugs): OTC or prescribed
104
Q

Heat does what?

A
  • increases circulation
  • blood vessel dilation
  • reduces nociception and ischemia caused by muscle spasm
105
Q

Cold does what?

A
  • applied to inhibit pain
  • vasoconstriction and decrease blood flow into tissues decrease swelling
  • reduce muscle spasm
106
Q

Therapeutic electrical modality does what?

A
  • induce analgesia by targeting pain

- electrical stimulation agents used to target gate theory

107
Q

Pharmacological agents does what?

A
  • oral, injectable medications to combat inflammation
  • non-steroidal anti-inflammatory (NSAID) to decrease vasodilation and capillary permeability: to increase leukocytes to stay in capillaries
  • side effects
108
Q

Assist the natural process of the body while doing ___ ____.

A

no harm

109
Q

Primary goals in rehab plan:

A
  • positive influence on inflammation and repair process
  • minimize early effects of inflammatory process
  • expedite recovery of function
  • prevent recurrence of injury
110
Q

Early effects of inflammatory process:

A
  • pain
  • spasm
  • edema accumulation
  • decreased motion
111
Q

How to expedite recovery of function:

A
  • pain-free movement/ROM
  • full extensibility of associated muscles and joint
  • acquiring full strength
  • cardiorespiratory fitness
  • neuromuscular control
112
Q

How to prevent recurrence of injury:

A

resist future periods of tissue overload through strengthening

113
Q

PLAN for acute injury phase:

A
  • initial swelling management and pain control are crucial (PRICE/POLICE)
  • immobilize initially 24-48 hours
  • by days 3-4, begin to engage in some mobility exercises (weight bear)
  • pain management tools
114
Q

PLAN for repair phase:

A
  • increase cardiorespiratory fitness
  • restore full ROM
  • restore or increase strength
  • re-establish neuromuscular control
  • add exercises (modifications, CKC)
  • continued pain modulation and swelling control (cryotherapy, electrical stimulation)
115
Q

PLAn for remodelling phase:

A
  • longest phase
  • ultimate goal = return to function
  • continued collagen realignment (ongoing healing processes)
  • pain continues to decrease with activity, limited swelling
  • regain activity specific skills (dynamic functional activities, strengthening, plyometric strength)
  • functional testing to determine specific skill weakness
  • continued use of tools or modalities pending goals (increase circulation to deeper tissues: heat, roller, massage)
116
Q

Why do we want to increase circulation to deeper tissues in the remodelling phase?

A

enhanced and lymphatic flow will deliver essential nutrients and increase breakdown/removal of waste

KIN 440 (10 decks)

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