interventions final Flashcards
focus of physical stress theory
how all biological tissues react and adapt to varied levels of physical stress, or lack thereof, are imparted upon them
thresholds for adaptations
injury
increased tolerance
decreased tolerance
in which level do tissues have no change
maintenance
what happens with stressors that are below maintenance?
change in tissue and decreased tolerance
what happens with stressors that are at maintenance?
no change in tissue or tolerance
what happens with stressors that are above maintenance?
change in tissue and increased tolerance
what happens with stressors that are far above maintenance?
injury or tissue failure
are stressors isolated or cumulative?
cumulative
the composite value of stress contains what components?
time, magnitude, and direction of overall stress application
overall stress exposure if affected by what?
history of recent stresses
movement and alignment factors
muscle performance
motor control
posture and alignment
physical activity
occupational, leisure, and self-care activities
extrinsic factors
orthotic devices, taping, ADs
footwear
ergonomic environment
modalities
gravity
physiological factors
medication
age
systemic pathology
obesity
physical stress level is …
a composite value
3 injury mechanisms
high-magnitude stress applied for a brief time
low-mag stress applied for a long duration
moderate-mag stress applied to tissue repeatedly
stimulus - recovery - adaptation
immediately following stressor, there is inflammatory response which renders the tissue less stress tolerate until recovery occurs
what happens if stress was significant magnitude and tissue properly recovers?
the tissue will be more resilient that previosly
another word for significant magnitude
overloading
what is the effect of progressive underload?
doing less needs lower set-points for thresholds
what is the effect of progressive overload?
doing more needs higher set-points for thresholds
what is the PT’s role in PST?
modify the stresses to achieve a desired goal
pain and dysfunction have a huge psychobiosocial component!
3 questions to apply to exercise and activity tolerance
what is the activity goal?
what are current modifiable factors limiting goal?
how should these factors be modified to meet the goal?
what is mechanotransduction?
cells sense and respond to mechanical loads converting mechanical loading to cellular responses
what do cellular responses promote?
structural change
what cell types sense and respond to mechanical stimuli?
osteocytes
chondrocytes
fibroblasts
keratinocytes
stem cells
what part of most cells types are mechanosensitive and responsive?
primary cilium
mechano-coupling
mechanical trigger or catalyst
what happens during mechano-coupling?
the physical load causing a physical perturbation to cells that make up a tissue
occurs in numerous cells in a given tissue
cell-cell communication
communication throughout a tissue to distribute the loading message via cell signaling
what happens during cell-cell communication?
cells are physically intact throughout the tendon.
what are gap junctions?
specialized regions where cells connect and communicate charged particles.
CCC
effector response
response at the cellular level = tissue factory that produces and assembles the necessary materials in the correct alignment
what happens during effector response?
mechanical loading stimulates protein synthesis at the cellular level.
what do integrin proteins do?
bridge the intracellular and extra-cellular regains, and cytoskeleton, which functions to maintain cells integrity and distribute mechanical load
2 distinct pathways that integrin proteins activate?
cytoskeleton is in direct physical communication with nucleus
biochemical signaling agents - influence gene expression in the nucleus
summary of effector cell response
mechanical stimulus on outside of cell promotes intracellular processes leading to matrix remodeling.
PST in absence of activity
mechanotranduction signal is weak, so connective tissue of lost
ex. osteoporosis in bone
PST when loads are above tissue’s set point
body adapts by increasing protein synthesis and adding tissue where possible
are tendons mechanoresponsive?
they are very mechanoresponsive
higher intensity of loading, greater morphological change and stiffness induced
mechano-tranduction in muscles
pivotal in the regulation of protein synthesis, calcium balance, contractility and muscle mass
where does the change happen in muscles?
z discs
anabolic response to tension
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
acute tissue healing
beings with inflammatory response and progresses until healing is complete and tissue is remodeled
inflammatory phase
damaged cells initiate inflam response
injury by-products removed by leukos
prepares tissue for proliferative
day 0 - day 4
cardinal signs of inflammation
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
proliferation phase
granulation tissue forms
tissue integrity is restored, strength not at peak yet
day 4 - week 2-6
repar and remodeling
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
what to use to cool tissues down?
cryotherapy
what can I do in inflam stage 1 of healing?
mostly pain free ROM
sig pain may further damage the tissue
promote muscle contraction
PRICE
PROM, AAROM, possibly AROM
two pathways in remodeling
reabsorption of early predominantly type III collagen and replacement with predominantly type I collagen
OR
reorientation of collagen fibers
what can we do at stage II of healing?
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
type I collagen
found in body
most abundant in body
type II collagen
found in cartilage
type III collagen
found in intestines, muscles, blood vessels, uterus
what happens to fibers doing stage III
align to the stresses applied to them
stresses assist through mechano-transduction
pain
protective mechanism to indicate tissue damage
inflammation
natural process to address issue
edema
secondary result of inflammatory process
acute pain goals
decrease pain
control inflam and edema
protect from further damage
increase ROM and function
immobilization in acute
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
early ROM can
reduce atrophy in musculature
maintain joint function
prevent lig creeping
reduce occurence of excessive scarring
enhance cartilage nutrition and vascularization
progressive controlled mobility
bone and ST responds to mechanical tension and will remodel/realign along the lines of tensile force
therapeutic benefits of movement
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
chronic inflam
when acute response is not sufficient to eliminate injuring agent
osis = chronic
itis = acute
what do isometric allow
force generation without change in ROM
very good for pain modulation
passive ROM
controlled
mostly pain free
cues for deep breathing to prevent guarding
more secure with more contact points
AAROM -> AROM
can modify position to affect line of force of gravity
ankle acute
iso - against surface
early AROM/AAROM - abcs
knee acute
iso - theraband
AROM/AAROM - bike, heel slides
hip acute
iso - yoga ball
AROM/AAROM - clam shell, bent knee fall out, windshield wipers
PNF patterns
elbow/wrist acute
iso - hold bar bell
ROM tool - juxtisizer
shoulder acute
PROM - cane, pulley, codman’s pendulum
AAROM/AROM - slides, quadruped
cervical acute
iso - with hand
chin tuck
with laser
thoracic/lumbar acute
iso holds
quadruped
knees to chest
rotations - watch trunk
as soon as inflam is controlled:
maintain or incres cardiorespiratory fitness
restore full ROM
restore or incres strength
reestablish NM control
what should the prescribed exercise program do?
challenge neural, muscular, and articular systems that help to regain NM control
as NM control improves:
strength will improve with it
after neural injury:
pt must relearn how to integrate visual, proprioception and kinematic info to produce movement
what can we do in sub-acute
begin resisted ROM (con and ecc strengthening)
initiate stretching with load at end range if needed
what ROM do you use?
depends on tissues in question and source of mobility limitation
what is required or desired adaptation according to pts needs?
absolute strength
muscular endurance
motor control
ROM
balance
COMBO
where to start in sub acute?
have a baseline of joint stability and NM motor control
base on pt needs
motor learning: three phases
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
why NM control first?
force that cannot be controlled by muscle will transmit to surrounding ST
increased injury risk
early exercise prescription
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
what do you progress/regress
strength - load
endurance - reps
coordination - complexity
dual-task - spatial and cognitive demands
regressions
lighter weight
slower speed
lower volume of sets/reps
lower frequency
predictable
simple
stable
more rest
progressions
heavier weight
faster speed
higher vol of reps/sets
higer freq
unpredictable
complex
unstable
less rest
what to investigate if pt has balance deficits?
weakness
endurance
coordination
dual task/cog deficits
tissue disruption
vestibular deficits
somatosensory deficits - neuropathy
poor kines awareness
challenging balance and stability
utilizing unstable surfaces good for balance
unstable surfaces not good to increase force production - incres tissue injury
stabilization continuum (most - least)
floor
sport beam
half foam roll
airex pad
dyna disc
stabilization continuum lower body (most - least)
two leg stable
staggered stance stable
single leg stable
two leg unstable
staggered unstable
single led unstable
stabilization continuum upper body (most - least)
two arm
alternating arms
single arm
single arm with trunk rotation
ligament structure
dense CT in parallel bundles
more flattened than tendons
ligament function
stability
position control in joint articulation
proprioceptive input
grade 1 lig sprain
stretch lig with microscopic tearing
grade 2 lig sprain
partial tearing
grade 3 lig sprain
complete rupture
what happens with complete rupture?
presence of gross laxity
likely nerves are involved
lig healing
up to 72 hours - blood loss and inflam
next 6 weeks - collagen put down
lig injury reoccurance
high
maturation of scar may take up to 12 months to complete
factors affecting lig healing
surgically repaired are stronger
scarring lengthens the lig
cartilage structure
rigid CT
what proteins trap water in cartilage?
proteogylcans
glycosaminoglycans
hyaline cartilage
found in nose
large collagen and proteoglycan
fibrocartilage
able to withstand high pressures
elastic cartilage
most flexible
stages of osteoarthritis
stage 1: 10% cartilage loss
2: joint space narrowing, osteophytes
3: gaps in cartilage expand until they reach bone
4: 60% cartilage loss
articular cartilage defect
0: intact
1: chondral softening or blistering
2: involves less than 50%
3: involves 50% or more
4: full thickness, bone on bone
cartilage breakdown
if not exposed to weight bearing, more likely to fibrillate
if stressors too high, cause microfractures
chrondromalacia
cartilage softening in weightbearing areas
cartilage healing
limited blood supply causes limited healing
describe CT in bone
shaft with articular surfaces lined with hyaline cartilage
bone healing
has adequate blood supply
open fracture
displacement of fractured ends that breach skin
closed fracture
little or no displacement
no skin breach
stress fracture
found in weight bearing bones
repetitive forces produce micro fractures
do not show up on x rays
fracture healing
hematoma formation
soft callus formation
hard callus formation
bone remodeling
four skeletal muscle characteristics
elasticity - Lengthen
extensibility - shorten
excitability - respond to stim
contractility - shorten and contract
muscle strain
when overstretched or forced to contract against too much resistance
most common in large muscles
muscle strain grades
1: <5% tear
2: partial tear ~50%
3: complete rupture
physiology of muscle healing
longer than other tissues
active contraction under load is essential
type 1 muscle soreness
transient muscle soreness immediately after exercise
type 2 muscle soreness
DOMS
approximately 12 hrs after injury
peak 24-48 hrs
resolves in 3-4 days
what actions cause greater DOMS
eccentric
lactate hypothesis
lactate does not cause DOMS
tendonitis
imflam within tendon without inflam of paratendon
tendinosis
significant degeneration without signs of histological inflam response
crepitus
adherence of paratendon as it slides back and fourth
treating tendonitis
REST
controlled loading
tenosynovitis
synovial sheath inflam
causes tendon to adhere to sheath
physiology of tendon healing
must do the right thing at the right time
excessive collagen leads to adhesions
