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fall A 2024 > interventions final > Flashcards

interventions final Flashcards

1
Q

focus of physical stress theory

A

how all biological tissues react and adapt to varied levels of physical stress, or lack thereof, are imparted upon them

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2
Q

thresholds for adaptations

A

injury
increased tolerance
decreased tolerance

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3
Q

in which level do tissues have no change

A

maintenance

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4
Q

what happens with stressors that are below maintenance?

A

change in tissue and decreased tolerance

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5
Q

what happens with stressors that are at maintenance?

A

no change in tissue or tolerance

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6
Q

what happens with stressors that are above maintenance?

A

change in tissue and increased tolerance

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7
Q

what happens with stressors that are far above maintenance?

A

injury or tissue failure

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8
Q

are stressors isolated or cumulative?

A

cumulative

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9
Q

the composite value of stress contains what components?

A

time, magnitude, and direction of overall stress application

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10
Q

overall stress exposure if affected by what?

A

history of recent stresses

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11
Q

movement and alignment factors

A

muscle performance
motor control
posture and alignment
physical activity
occupational, leisure, and self-care activities

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12
Q

extrinsic factors

A

orthotic devices, taping, ADs
footwear
ergonomic environment
modalities
gravity

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13
Q

physiological factors

A

medication
age
systemic pathology
obesity

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14
Q

physical stress level is …

A

a composite value

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15
Q

3 injury mechanisms

A

high-magnitude stress applied for a brief time
low-mag stress applied for a long duration
moderate-mag stress applied to tissue repeatedly

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16
Q

stimulus - recovery - adaptation

A

immediately following stressor, there is inflammatory response which renders the tissue less stress tolerate until recovery occurs

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17
Q

what happens if stress was significant magnitude and tissue properly recovers?

A

the tissue will be more resilient that previosly

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18
Q

another word for significant magnitude

A

overloading

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19
Q

what is the effect of progressive underload?

A

doing less needs lower set-points for thresholds

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20
Q

what is the effect of progressive overload?

A

doing more needs higher set-points for thresholds

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21
Q

what is the PT’s role in PST?

A

modify the stresses to achieve a desired goal

pain and dysfunction have a huge psychobiosocial component!

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22
Q

3 questions to apply to exercise and activity tolerance

A

what is the activity goal?
what are current modifiable factors limiting goal?
how should these factors be modified to meet the goal?

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23
Q

what is mechanotransduction?

A

cells sense and respond to mechanical loads converting mechanical loading to cellular responses

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24
Q

what do cellular responses promote?

A

structural change

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25
Q

what cell types sense and respond to mechanical stimuli?

A

osteocytes
chondrocytes
fibroblasts
keratinocytes
stem cells

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26
Q

what part of most cells types are mechanosensitive and responsive?

A

primary cilium

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27
Q

mechano-coupling

A

mechanical trigger or catalyst

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28
Q

what happens during mechano-coupling?

A

the physical load causing a physical perturbation to cells that make up a tissue

occurs in numerous cells in a given tissue

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29
Q

cell-cell communication

A

communication throughout a tissue to distribute the loading message via cell signaling

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30
Q

what happens during cell-cell communication?

A

cells are physically intact throughout the tendon.

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31
Q

what are gap junctions?

A

specialized regions where cells connect and communicate charged particles.

CCC

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32
Q

effector response

A

response at the cellular level = tissue factory that produces and assembles the necessary materials in the correct alignment

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33
Q

what happens during effector response?

A

mechanical loading stimulates protein synthesis at the cellular level.

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34
Q

what do integrin proteins do?

A

bridge the intracellular and extra-cellular regains, and cytoskeleton, which functions to maintain cells integrity and distribute mechanical load

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35
Q

2 distinct pathways that integrin proteins activate?

A

cytoskeleton is in direct physical communication with nucleus

biochemical signaling agents - influence gene expression in the nucleus

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36
Q

summary of effector cell response

A

mechanical stimulus on outside of cell promotes intracellular processes leading to matrix remodeling.

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37
Q

PST in absence of activity

A

mechanotranduction signal is weak, so connective tissue of lost

ex. osteoporosis in bone

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38
Q

PST when loads are above tissue’s set point

A

body adapts by increasing protein synthesis and adding tissue where possible

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39
Q

are tendons mechanoresponsive?

A

they are very mechanoresponsive

higher intensity of loading, greater morphological change and stiffness induced

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40
Q

mechano-tranduction in muscles

A

pivotal in the regulation of protein synthesis, calcium balance, contractility and muscle mass

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41
Q

where does the change happen in muscles?

A

z discs

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42
Q

anabolic response to tension

A

myofibers are capable of differentiating between chronic longitudinal tension

producing growth in length through sarcomere deposition in series, and chronic functional overload, which produces cross-sectional hypertrophy

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43
Q

acute tissue healing

A

beings with inflammatory response and progresses until healing is complete and tissue is remodeled

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44
Q

inflammatory phase

A

damaged cells initiate inflam response
injury by-products removed by leukos
prepares tissue for proliferative

day 0 - day 4

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45
Q

cardinal signs of inflammation

A

heat - vasodilation
redness - vasodil
swelling - incres vascular permeability, granulation tissue
pain - physical and chemical stim of nociceptors
loss of function - pain, reflex muscle inhibition, disruption of tissue structure, fibroplasia and metaplasia

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46
Q

proliferation phase

A

granulation tissue forms
tissue integrity is restored, strength not at peak yet

day 4 - week 2-6

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47
Q

repar and remodeling

A

ongoing
decres in type III and cres in type I
collagen in wound matures and strengthens
max strength of new tissue regained in this phase around 4-5 weeks

week 2 - ongoing up to 18 months after wound closure

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48
Q

what to use to cool tissues down?

A

cryotherapy

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49
Q

what can I do in inflam stage 1 of healing?

A

mostly pain free ROM
sig pain may further damage the tissue
promote muscle contraction
PRICE
PROM, AAROM, possibly AROM

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50
Q

two pathways in remodeling

A

reabsorption of early predominantly type III collagen and replacement with predominantly type I collagen

OR

reorientation of collagen fibers

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51
Q

what can we do at stage II of healing?

A

tissue stressors should be gradual with continuous monitoring
signs of further tissue damage encourage reassessment of healing timeframes

we want to safely stress but not cause anymore damage

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52
Q

type I collagen

A

found in body

most abundant in body

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53
Q

type II collagen

A

found in cartilage

54
Q

type III collagen

A

found in intestines, muscles, blood vessels, uterus

55
Q

what happens to fibers doing stage III

A

align to the stresses applied to them
stresses assist through mechano-transduction

56
Q

pain

A

protective mechanism to indicate tissue damage

57
Q

inflammation

A

natural process to address issue

58
Q

edema

A

secondary result of inflammatory process

59
Q

acute pain goals

A

decrease pain
control inflam and edema
protect from further damage
increase ROM and function

60
Q

immobilization in acute

A

controlled mobilization is better

brief immo during inflam recommended and can facilitate healing by controlling inflam

controlled activity to return to normal flexibility and strength combined with support or bracing

61
Q

early ROM can

A

reduce atrophy in musculature
maintain joint function
prevent lig creeping
reduce occurence of excessive scarring
enhance cartilage nutrition and vascularization

62
Q

progressive controlled mobility

A

bone and ST responds to mechanical tension and will remodel/realign along the lines of tensile force

63
Q

therapeutic benefits of movement

A

mech stim assist in pain reduction
stimulate endogenous endorphins for pain control
decrease in intra-articular pressure
improved joint mobility
positive effects on CT remodeling
beneficial gliding of tendons within sheaths

64
Q

chronic inflam

A

when acute response is not sufficient to eliminate injuring agent

osis = chronic
itis = acute

65
Q

what do isometric allow

A

force generation without change in ROM

very good for pain modulation

66
Q

passive ROM

A

controlled
mostly pain free
cues for deep breathing to prevent guarding
more secure with more contact points

67
Q

AAROM -> AROM

A

can modify position to affect line of force of gravity

68
Q

ankle acute

A

iso - against surface
early AROM/AAROM - abcs

69
Q

knee acute

A

iso - theraband
AROM/AAROM - bike, heel slides

70
Q

hip acute

A

iso - yoga ball
AROM/AAROM - clam shell, bent knee fall out, windshield wipers
PNF patterns

71
Q

elbow/wrist acute

A

iso - hold bar bell
ROM tool - juxtisizer

72
Q

shoulder acute

A

PROM - cane, pulley, codman’s pendulum
AAROM/AROM - slides, quadruped

73
Q

cervical acute

A

iso - with hand
chin tuck
with laser

74
Q

thoracic/lumbar acute

A

iso holds
quadruped
knees to chest
rotations - watch trunk

75
Q

as soon as inflam is controlled:

A

maintain or incres cardiorespiratory fitness
restore full ROM
restore or incres strength
reestablish NM control

76
Q

what should the prescribed exercise program do?

A

challenge neural, muscular, and articular systems that help to regain NM control

77
Q

as NM control improves:

A

strength will improve with it

78
Q

after neural injury:

A

pt must relearn how to integrate visual, proprioception and kinematic info to produce movement

79
Q

what can we do in sub-acute

A

begin resisted ROM (con and ecc strengthening)
initiate stretching with load at end range if needed

80
Q

what ROM do you use?

A

depends on tissues in question and source of mobility limitation

81
Q

what is required or desired adaptation according to pts needs?

A

absolute strength
muscular endurance
motor control
ROM
balance

COMBO

82
Q

where to start in sub acute?

A

have a baseline of joint stability and NM motor control

base on pt needs

83
Q

motor learning: three phases

A

cognitive: attention, overcorrection, poor quality, stiff movement, focus on performance

associative: refinement, less overcorrection, errors reduce, less cog attention needed

autonomous: little cog guidance, focus on unrelated topics

84
Q

why NM control first?

A

force that cannot be controlled by muscle will transmit to surrounding ST

increased injury risk

85
Q

early exercise prescription

A

low loads - safe and controlled
high reps - aids in reconditioning
controlled ROM
feedback/performance - prevents bad habits

safest repetition to begin?
slow to mod concen, slow and controlled ecen with full pause between

86
Q

what do you progress/regress

A

strength - load
endurance - reps
coordination - complexity
dual-task - spatial and cognitive demands

87
Q

regressions

A

lighter weight
slower speed
lower volume of sets/reps
lower frequency
predictable
simple
stable
more rest

88
Q

progressions

A

heavier weight
faster speed
higher vol of reps/sets
higer freq
unpredictable
complex
unstable
less rest

89
Q

what to investigate if pt has balance deficits?

A

weakness
endurance
coordination
dual task/cog deficits
tissue disruption
vestibular deficits
somatosensory deficits - neuropathy
poor kines awareness

90
Q

challenging balance and stability

A

utilizing unstable surfaces good for balance

unstable surfaces not good to increase force production - incres tissue injury

91
Q

stabilization continuum (most - least)

A

floor
sport beam
half foam roll
airex pad
dyna disc

92
Q

stabilization continuum lower body (most - least)

A

two leg stable
staggered stance stable
single leg stable
two leg unstable
staggered unstable
single led unstable

93
Q

stabilization continuum upper body (most - least)

A

two arm
alternating arms
single arm
single arm with trunk rotation

94
Q

ligament structure

A

dense CT in parallel bundles
more flattened than tendons

95
Q

ligament function

A

stability
position control in joint articulation
proprioceptive input

96
Q

grade 1 lig sprain

A

stretch lig with microscopic tearing

97
Q

grade 2 lig sprain

A

partial tearing

98
Q

grade 3 lig sprain

A

complete rupture

99
Q

what happens with complete rupture?

A

presence of gross laxity
likely nerves are involved

100
Q

lig healing

A

up to 72 hours - blood loss and inflam
next 6 weeks - collagen put down

101
Q

lig injury reoccurance

A

high

maturation of scar may take up to 12 months to complete

102
Q

factors affecting lig healing

A

surgically repaired are stronger
scarring lengthens the lig

103
Q

cartilage structure

A

rigid CT

104
Q

what proteins trap water in cartilage?

A

proteogylcans
glycosaminoglycans

105
Q

hyaline cartilage

A

found in nose

large collagen and proteoglycan

106
Q

fibrocartilage

A

able to withstand high pressures

107
Q

elastic cartilage

A

most flexible

108
Q

stages of osteoarthritis

A

stage 1: 10% cartilage loss
2: joint space narrowing, osteophytes
3: gaps in cartilage expand until they reach bone
4: 60% cartilage loss

109
Q

articular cartilage defect

A

0: intact
1: chondral softening or blistering
2: involves less than 50%
3: involves 50% or more
4: full thickness, bone on bone

110
Q

cartilage breakdown

A

if not exposed to weight bearing, more likely to fibrillate
if stressors too high, cause microfractures

111
Q

chrondromalacia

A

cartilage softening in weightbearing areas

112
Q

cartilage healing

A

limited blood supply causes limited healing

113
Q

describe CT in bone

A

shaft with articular surfaces lined with hyaline cartilage

114
Q

bone healing

A

has adequate blood supply

115
Q

open fracture

A

displacement of fractured ends that breach skin

116
Q

closed fracture

A

little or no displacement
no skin breach

117
Q

stress fracture

A

found in weight bearing bones
repetitive forces produce micro fractures

do not show up on x rays

118
Q

fracture healing

A

hematoma formation
soft callus formation
hard callus formation
bone remodeling

119
Q

four skeletal muscle characteristics

A

elasticity - Lengthen
extensibility - shorten
excitability - respond to stim
contractility - shorten and contract

120
Q

muscle strain

A

when overstretched or forced to contract against too much resistance
most common in large muscles

121
Q

muscle strain grades

A

1: <5% tear
2: partial tear ~50%
3: complete rupture

122
Q

physiology of muscle healing

A

longer than other tissues
active contraction under load is essential

123
Q

type 1 muscle soreness

A

transient muscle soreness immediately after exercise

124
Q

type 2 muscle soreness

A

DOMS
approximately 12 hrs after injury
peak 24-48 hrs
resolves in 3-4 days

125
Q

what actions cause greater DOMS

A

eccentric

126
Q

lactate hypothesis

A

lactate does not cause DOMS

127
Q

tendonitis

A

imflam within tendon without inflam of paratendon

128
Q

tendinosis

A

significant degeneration without signs of histological inflam response

129
Q

crepitus

A

adherence of paratendon as it slides back and fourth

130
Q

treating tendonitis

A

REST
controlled loading

131
Q

tenosynovitis

A

synovial sheath inflam
causes tendon to adhere to sheath

132
Q

physiology of tendon healing

A

must do the right thing at the right time

excessive collagen leads to adhesions

fall A 2024 (10 decks)

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