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FCA > MIDTERM (inflammatory process, wounds & burns, spasms, scar tissue, trigger points) > Flashcards

MIDTERM (inflammatory process, wounds & burns, spasms, scar tissue, trigger points) Flashcards

1
Q

what is the inflammatory process?

A

part of healing injured tissue

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2
Q

ultimate goal of the inflammatory process

A

promote a strong, mobile scar, possible full pain-free movement, full strength

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3
Q

causes of tissue damage

A

internal / external
common causes: trauma, infection, immune response, extreme heat/ cold, ischemic damage, radiation damage

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4
Q

re-epithelialization

A

replication of missing cells

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5
Q

granulation tissue

A

fibroblasts synthesize collagen that form loose CT matrix (1st / 2nd intention healing)

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6
Q

scar tissue

A

mature collagen repair

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7
Q

primary / first intention healing

A

occurs when there is some tissue loss & wound edges are approximated - healing is efficient with only small amounts of collagen produced to repair tissue

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8
Q

secondary / second intention healing

A

when there is extensive tissue loss / large area affected, wound edges cannot be bought together easily - healing takes longer through re-epithelialization

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9
Q

factors that affect the healing process

A

-severity of injury
-age
-infection
-presence of foreign material
-nutritional support
-existing conditions
-adequate blood supply
-wound separation
-effects of some drugs
-smoking

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10
Q

ACUTE STAGE

A

from moment of injury up to 3/4 days post-injury
redness, swelling, heat, pain, possible loss of function, muscle spasm & guarding, bruising (purple, blue, red)

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11
Q

ACUTE treatment goals

A

-limit inflammatory process
-reduce pain & swelling
-decrease SNS firing
-prevent re-injury
-protective spasms reduced but not removed
-compensatory structures treated

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12
Q

STAGES OF HEALING

A

acute
early subacute
late subacute
chronic

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13
Q

EARLY SUBACUTE STAGE

A

within two days of injury and may continue for up to 3 weeks
diminished signs of inflammation, pink, warm tissue, less pain, muscle spasm diminished, bruising unchanged

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14
Q

EARLY SUBACUTE treatment goals

A

-continue to decrease effects of inflammation, pain, swelling, & spasms
-maintain available ROM & strength

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15
Q

ACUTE hydrotherapy

A

cold application

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16
Q

EARLY SUBACUTE hydrotherapy

A

cold applications - introduction of mild contrast

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17
Q

LATE SUBACUTE STAGE

A

begins 2-3 weeks after
may be pocket of residual swelling, minimal discomfort, potential loss of ROM due to adhesions & muscle weakness, if bruising: yellow, green, brown

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18
Q

LATE SUBACUTE treatment goals

A

-decrease remaining edema
-reduce trigger points, pain & adhesions
-improve ROM & muscle strength

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19
Q

LATE SUBACUTE hydrotherapy

A

hot & cold contrast applications

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20
Q

CHRONIC STAGE

A

about 2-3 weeks post injury & continues for up to 1-2 years
inflammatory process resolved, likely no edema, potential loss of ROM & decrease in function, may be pain with overpressure

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21
Q

CHRONIC treatment goals

A

-reduce restrictive adhesions & trigger point
-restore ROM & strength to affected areas
-treating compensatory areas

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22
Q

CHRONIC hydrotherapy

A

hot & cold contrast applications

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23
Q

what is an injury?

A

disruption of the continuity of any tissue

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24
Q

epidermis

A

outer layer of skin
cell have short life span (28-30 days) which results in continuous sloughing off & renewal

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25
Q

dermis

A

beneath epidermis
anchors & nutritionally support
composed of elastin & collagen which gives tissue flexibility & strength
contains sebaceous & sweat glands, hair follicles, nerve receptors, blood & lymphatic vessels

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26
Q

subcutaneous

A

contains adipose tissue, larger blood vessels & deep hair follicles
below this layer are muscles & bone

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27
Q

what is a wound?

A

disruption of the continuity of skin

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28
Q

causes of wounds

A

thermal sources
chemical & electrical sources
mechanical forces - trauma, pressure, shear, friction force

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29
Q

types of wounds

A

-abrasion
-laceration
-incision
-puncture
-animal bite

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30
Q

abrasion

A

superficial wound, ragged edges
result of scrape / tear causing loss of skin
often extremely painful

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31
Q

laceration

A

increased tissue loss with ragged wound edges
sutures / tape may be used to bring edges together

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32
Q

incision

A

clean, approximated wound edges
results from sharp-edged object
sutures / tape used to secure edges together

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33
Q

puncture wound

A

clean edges with small entry, can penetrate deeply
can close over at entry before rest of damage heals: increased risk of infection

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34
Q

animal bite

A

combination of crush, laceration & puncture wound

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35
Q

what is a burn?

A

specific type of wound caused by external thermal agent

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36
Q

types of burns

A

-superficial burn
-partial-thickness burn
-full-thickness burn

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37
Q

superficial burn

A

first degree burn
effects epidermis
result of prolonged exposure to low heat / quick high heat
some mild localized edema
healing is rapid without scar tissue

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38
Q

partial thickness burn

A

second degree burn
extends to dermis
redness, pain, localized edema, blistering
increased edema & risk of infection
less pain due to nerve damage
can re-epithelialize with good function & minimal scar tissue

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39
Q

full thickness burn

A

third/ fourth degree burn
damage to all layers
dry, inelastic, white, waxy, charred in colour
painless because of nerve damage
re-epithelialize not possible (skin grafts required)

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40
Q
A
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41
Q

“rule of nines”

A

% of body surface damaged by burn

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42
Q

hypertrophic scar

A

destruction of collagen combined with contraction of myofibroblasts causes “heaped up” appearance of scar

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43
Q

complications of burns

A

-breathing
-inhalation injuries
-GI complications
-renal complications
-heterotrophic calcification
-burned skin
-thermoregulation impairment
-peripheral vascular damage
-sensory impairment/ loss
-subluxation & dislocation
-amputation

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44
Q

CI’s for burns

A

-infection risk: wash hands, gloves, oil not used around wound
-avoid direct contact with burns that produce blisters
-pressure directed toward injury site (acute)

45
Q

acute & early subacute: TREATMENT CONSIDERATIONS

A

-promote relaxation
-reduce pain
-reduce edema
-prevent infection
-encourage activity

46
Q

acute & early subacute: MASSAGE

A

-diaphragmatic breathing
-massage to unaffected areas (promote relaxation & stress reduction)
-affected limb elevated, massage proximal to injury
-distally, only techniques that do not increase circulation

47
Q

late subacute & chronic: TREATMENT CONSIDERATIONS

A

-reduce any remaining edema
-decrease SNS firing
-decrease pain
-increase local circulation
-reduce adhesions
-improve ROM

48
Q

late subacute & chronic: MASSAGE

A

-diaphragmatic breathing
-edema treated if present
-massage proximal to injury site
-decrease adhesions
-STRETCH scar tissue
-hydro: warm, prior to stretching, cold: decrease pain
-joint play

49
Q

what is a spasm?

A

involuntary, sustained contraction of a muscle

50
Q

what is a cramp?

A

painful, prolonged muscle spasm

51
Q

reflex muscle guarding

A

muscle spasm in response to pain, due to local injury & is present in acute stages

52
Q

intrinsic muscle spasm

A

involuntary self-perpetuating pain-spasm cycle
-pain from direct/ indirect trauma, infection, increase in SNS, emotional stress, cold tissue

53
Q

tone

A

resistance of relaxed muscle to passive stretch / elongation

54
Q

tension

A

muscle fibers tend to shorten, causing them to perform work

55
Q

hypertonicity

A

abnormally high tone usually seen with upper motor neuron disorders

56
Q

how does a muscle contract?

A

-skeletal muscle = bundle of fascicles (grouping of muscle fibers) -> made up of thousands of fine strands = myofibrils -> contains thick & thin filaments arranged in units that repeat along myofibil = sarcomere (basic contractile units of muscle fibers)
-thick filaments (myosin) & thin filaments (actin) overlap and produce contractile force, slide past & shorten sarcomere -> repeated actions = MUSCLE CONTRACTION

57
Q

two structures in spasms

A

muscle spindles & golgi tendon organ (GTO): transmit proprioceptive information from muscles to CNS to allow proper muscle function

58
Q

muscle spindles

A

major sensory organs of muscles & aid in control of muscle movements (in muscle belly)
-measure degree (length) & speed a muscle is stretched

59
Q

golgi tendon organ (GTO)

A

nerve receptors located near their muscular attachments
-sensitive to tension
-when they fire, they inhibit contraction of muscle
-protect muscle from overstretch injury

60
Q

causes of muscle spasms & cramps

A

-pain
-circulatory stasis
-increased gamma neuron firing
-chilling of muscle
-impaired nutrition supply
-lack of vitamin D

61
Q

symptom picture of spasms & cramps

A

-pain within muscle (ischemia & retention of metabolites)
-spasm & hypertonicity present
-decreased ROM of joint
-antagonist & synergist affected
-TP’s in other muscles may refer

62
Q

H.H questions (spasms)

A

-general health / contributing factors
-previous injury
-pain: where / quality
-precipitating factors
-onset
-medications

63
Q

palpation (spasms)

A

-affected muscle: hot = acute congestions, cold = ischemia
-point tender due to ischemia
-texture of acutely spasmodic muscle = firm, dense, congested
-texture of intrinsic muscle = hard & fibrous
-affected muscle is hypertonic, as well as synergist & antagonist

64
Q

contraindications

A

-DO NOT attempt to completely eliminate reflex muscle guarding that is splinting acute injury
-avoid passively stretching acutely spasmodic muscle
-hot hydro CI’d with spasm from acute injury
-massage locally CI’d with DVT

65
Q

treatment GOALS (spasm)

A

-break pain-spasm cycle, decrease spasm
-if reflex muscle guarding, do NOT disturb healing process & decrease only portion of spasm present
-decrease pain & SNS
-increase local circulation
-decrease hypertonicity
-once spasm has been reduced, increase ROM

66
Q

TREATMENT (spasm)

A

-indirect techniques (GTO, O & I), direct techniques may be too painful
-massage to flush metabolites & decrease pain

67
Q

GTO technique (effectiveness)

A

on muscles whose tendons are long & easily palpable

68
Q

O & I technique (effectiveness)

A

used when tendon to be treated is short
(variation of GTO release)

69
Q

muscle approximation (effectiveness)

A

direct technique, lessens stretch on muscle spindles

70
Q

what is scar tissue?

A

fibrous, collagen based tissue that develops as a result of the inflammatory process
-scar tissue = weaker than tissue it replaces

71
Q

types of scar tissue

A

-contracture
-adhesion
-scar tissue adhesion
-fibrotic adhesion
-irreversible contracture
-proud flesh
-hypertrophic scarring
-keloid scar

72
Q

contracture

A

shortening of CT supporting structures around joint (muscles, tendons, joint capsules)
-tissue cannot fully lengthen, reduced ROM
(adhesions & irreversible contractures)

73
Q

adhesion

A

occurs when reduced motion at joint allows cross-links to form among collagen fibers, reducing ROM (when tissue is left in shortened position for prolonged periods of time)

74
Q

scar tissue adhesion

A

occurs with injury / acute inflammatory process
collagen fiber formation allows adhesions & contractures to form in random pattern, reducing ROM

75
Q

fibrotic adhesion

A

occurs with ongoing chronic inflammation that can cause moderate to severe restrictions in ROM (difficult to eradicate)

76
Q

irreversible contractures

A

occurs when fibrotic tissue / bone replaces muscle & CT
-permanent loss in ROM, can only be restored by surgical means

77
Q

proud flesh scar

A

thick dermal granulation tissue that results from abnormal healing process
-raised, red structure, susceptible to damage

78
Q

hypertrophic scarring

A

overgrowth of dermal tissue WITHIN boundaries of wound

79
Q

keloid scar

A

dermal scar tissue that extends BEYOND original wound, tumour-like growth
-may grow for years / recur

80
Q

effects of massage on scar tissue

A

-decrease edema before scar tissue develops = removes excess interstitial fluid, reduces amount of scar tissue that develops
-helps soften scar tissue by decreasing fibrotic adhesions & increasing circulation
-helps desensitize
-stretching scar tissue after massage is essential (*realign ribers)

81
Q

CONTRAINDICATIONS (scar tissue)

A

frictions are CI’d on: proud flesh / keloid scars, anti-inflammatory medications

82
Q

observations (scar tissue)

A

may be aneural (not innervated) / partially innervated
is avascular (no hair, sebaceous, sweat glands)

83
Q

palpation (scar tissue)

A

-scar tissue & adhesions = thick, hard areas
-may be cool due to ischemia
-disuse atrophy (muscle weakness) may be present / loss of ROM

84
Q

HYDRO (scar tissue)

A

-pre treatment: heat
-post treatment: cold (after frictions)

85
Q

GOALS (scar tissue)

A

-create mobile, functional scar
-periphery of scar treated first, then toward center
-cross-fiber frictions on adhesions
-techniques from least adhered to most adhered
-massage followed by passive stretch to promote alignment of collagen fibers

86
Q

cross-fiber frictions

A

-developed by James Cyriax
-intended to disrupt & break down existing & forming adhesions in muscles, tendons & ligaments using compression & motion
-used in subacute & chronic stages of healing to break down adhesions
-suggested 10-20 minutes effleurage before frictions performed

87
Q

what is a trigger point?

A

hyperirritable spot, within discrete taut band of skeletal muscle or its fascia that produces local & referred pain
-point tender on site, often predictable pain referral pattern
-causes affected muscle to shorten
-condition, not a method

88
Q

theory of what causes trigger points

A

-interaction of calcium & ATP on myofascial tissues that have been stressed in some way, causes tissue to shorten
-generates localized & uncontrolled metabolic activity
-localized acidic fluid environment -> makes nerve endings hyperirritable resulting in pain
-tiny microfilaments in muscles start to stick together (adhesions)

89
Q

myofascial pain syndrome

A

-most common form of muscle pain
-involves pain with specific “trigger” / “tender” points
-sensory, motor & autonomic symptoms occur
-can occur from soft tissue injury / when use of muscles exceed their ability & normal recovery is disturbed

90
Q

perpetuating factors (trigger points)

A

-reflexive
-mechanical
-systemic

91
Q

reflexive (trigger points)

A

-skin sensitive in area of TP
-joint dysfunction
-visceral dysfunction in referred pain pattern
-vasoconstriction
-facilitated nerve segment

92
Q

mechanical (trigger points)

A

-gait distortion
-immobilization
-vocational stress
-restrictive / ill-fitting clothing & stress
-furniture

93
Q

systemic (trigger points)

A

-enzyme dysfunction
-metabolic & endocrine dysfunction
-chronic infection
-dietary insufficiencies
-psychological stress

94
Q

types of trigger points

A

-active
-latent
-primary
-secondary
-satellite

95
Q

ACTIVE TP

A

-painful at rest & with active/ passive movement of muscle
-prevents muscle from fully lengthening & reduces its strength
-tissue ischemia
-palpation can produce local twitch response & possible referred autonomic phenomena

96
Q

LATENT TP

A

-opposite to active / more common
-produces pain only when palpated

97
Q

PRIMARY TP

A

directly activated by acute / chronic mechanical strain or overload of affected muscle

98
Q

SECONDARY TP

A

activated in overworked synergist / antagonist muscle

99
Q

SATTELITE TP

A

found in muscles that lie within referral pattern of another TP

100
Q

symptom picture (trigger points)

A

-pain / tenderness
-sensitivity of active TP can change over several hours / days
-passive stretching & contraction is painful
-possible autonomic symptoms
-palpable taut band
-decreased circulation in muscle local to TP
-decreased ROM
-synergists & antagonists affected
-muscle weakness

101
Q

observations (trigger points)

A

-antalgic gait may be present if TP is in lower torso / limb
-antalgic posture may be present with active TP
-client may have pained expression

102
Q

palpation (trigger points)

A

-referral patterns
two methods used: flat palpation & pincer palpation
-may feel like tiny nodule

103
Q

PANNICULOSIS

A

-thickening of subcutaneous tissue
-no inflammation present
-skin rolling useful to reveal

104
Q

JUMP SIGN

A

may occur where pain is intense enough to cause client to wince, jump, cry out

105
Q

CONRAINDICATIONS (trigger points)

A

-avoid vigorous techniques when treating hyperirritable TP’s since “kick-back” pain may result
-treating TP’s proximal to area with acute inflammation: heat = CI’d
-acute / early subacute (sprains/strains): treatment local to injury CI’d
-avoid prolonged chilling of muscle (may activate TP)
-avoid prolonged ischemic compressions & frictions
-full stretch after TP treatment is completely CI’d if crosses a hypermobile joint

106
Q

POST trigger point treatment

A

-stimulate circulation
-lengthening the muscle should be completed passively / actively
-moist heat immediately after treatment: soothing & useful

107
Q

methods of treating trigger points

A

-direct pressure / manipulation
-ice massage
-dry needling
-positional release
-muscle energy

108
Q

trigger point release techniques

A

-skin rolling
-muscle stripping
-alternate ischemic compressions
-variable pressure technique
-cross-fiber frictions

FCA (5 decks)

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