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goal
injury type
timeline (how recent)
considerations when choosing a therapeutic intervention/modality
inactive phase (shut down)
active phase
resistive phase
aggressive phase
rehabilitation phases
rehabilitation phase
rehabilitation phases where therapeutic modalities should be used for pain, spasm, and edema relief
active phase
rehabilitation phase for joint mobilization, soft tissue mobilization, ROM, and flexibility
resistive phase
rehabilitation phase for muscle strength and endurance exercises, proprioception and balance exercises for neuromuscular recovery
aggressive phase
rehabilitation phase for plyometric exercises, functional exercises, and performance-specific exercises for return to function
active phase
resistive phase
aggressive phase
rehabilitation phases that focus on therapeutic exercises
healing phases
inflammation
proliferation (early and late)
remodeling/maturation
stress
mechanical, thermal, emotional, or chemical force on the body
cell death
tissue response when physical stress level is none to low
decreased tolerance (atrophy)
tissue response when physical stress level is low
maintenance
tissue response when physical stress level is normal
increased tolerance (hypertrophy)
tissue response when physical stress level is moderate (positive overload)
injury
tissue response when physical stress level is high (chronic)
cell death
tissue response when physical stress level is extreme (acute, ex ACL)
alarm
resistance
exhaustion
general adaption syndrome stages
our stress response system defends, then fatigues
general adaption syndrome (GAS)
GAS Alarm stage physiology changes
fight or flight
increased HR
increased CO
increased SV
vasoconstriction
cortisol
GAS resistance phase
longest phase
adapts to stressor
intensity, duration
stress applied to body must be of proper ________ and __________
Wolff’s Law
bones adapts to the forces placed on it
osteoblast
builds bone
osteoclasts
absorb and remove unwanted bone
skin
intestinal tract
blood
labile cell tissue locations
good
labile cell ability to regenerate
bone
stabile cells tissue location
some
stabile cells ability to regenerate
muscle
PNS
CNS
permanent cells tissue locations
some
permanent cells located in muscle regenerative ability
some
permanent cells located in PNS regenerative ability
none
permanent cells located in CNS regenerative ability
skin
heart
blood vessels
hollow organs
glands
external openings
structures lined by epithelial tissue
stratum corneum
forms the skin’s outer later
keratin
what is the stratum corneum filled with?
skeletal
smooth
cardiac
muscle types
Type I
Type II
muscle fiber types
Type I - smaller diameter
muscle fiber type that is recruited faster
Type I
muscle fiber type slow to fatigue and prevalent in postural muscles
Type II
muscle fiber type capable of generating a high amount of force in a short time
brain
spinal cord
structures that make up CNS
peripheral nerves
structures that make up PNS
afferent signal
signal that travels away from the stimulus to the brain
efferent signal
signal that goes towards the stimulus
Ia (A-alpha)
Ib (A-alpha)
II (A-beta)
III (A-delta)
IV (C)
afferent axons
efferent axons
A-alpha
A-gamma
A-beta
muscle spindle afferent
Ia (A-alpha) axon function
golgi tendon afferent
Ib (A-alpha) axon function
touch/pressure afferent, secondary muscle afferent
II (A-beta) axon function
temperature afferent, sharp pain
III (A-delta) axon function
temperature afferent
dull pain
IV (C) axon function
skeletal muscle efferent
A-alpha axon function
muscle spindle efferent
A-gamma axon function
muscle and muscle spindle efferent
A-beta axon function
motor nerves
acetylcholine location
transmits motor impulse
acetylcholine functions
CNS
calcitonin gene-related peptide location
calcitonin gene-related peptide functions
vasodilation
activates leukocytes
reduces pain threshold
brain stem
dopamine location
dopamine absence consequences
motor dysfunction
increased BP
increased CO
vasoconstriction
brain stem
epinephrine location
behavior
bronchial dilation
emotions
mood
vasoconstriction
epinephrine affects:
autonomic nervous system
norepinephrine location
arousal
dreams
mood regulation
vasoconstriction
norepinephrine functions
platelets, mast cells
serotonin location
sensory perception
sleep
temperature regulation
vasoconstriction
serotonin functions
pain-transmitting nerve fibers
substance P location
transmits noxious impulses, produces inflammation-like responses in local tissues
substance P function
primary destruction
tissue destruction as a result of force or stress
secondary destruction
cell death or destruction as a result of primary injury
platelet accumulation, coagulation, leukocyte migration
what happens during the acute phase of healing?
fibroblastic repair
tissue growth
collagen matrix formation
what happens during the proliferation phase of healing?
more new tissue deposited, get tissue back to original function
what happens during the maturation/remodeling phase of healing?
neutrophils and macrophages
phagocytes and fibroblasts released during acute inflammation
phagocytes and fibroblasts released
formulation of granulation of tissue
hemorrhage
fibrin clot formation
histamine released
acute inflammatory response
increase cell permeability → increased swelling
histamine’s effect on traumatized cells
2-4 days post injury
acute inflammatory response duration
redness
swelling
tenderness
increased temperature
loss of function
cardinal signs of inflammation
acute
subacute
chronic
stages of inflammation
0-14 days
acute inflammation duration (acute vs subacute vs chronic)
14-31 days
subacute inflammation duration (acute vs subacute vs chronic)
>31 days after expected resolution
chronic inflammation timeline
heparin
histamine
kinins
neutrophils
prostaglandins
serotonin
leukotrienes
inflammatory mediators
heparin
histamine
kinins
prostaglandins
leukotrienes
pro-inflammatory inflammation mediators
neutrophils
serotonin
anti-inflammatory inflammation mediators
heparin
inflammatory mediator that inhibits coagulation by preventing the conversion of prothrombin to thrombin
histamine
inflammatory mediator that vasodilates arterioles and increases vascular permeability
kinins
inflammatory mediator that dilates arterioles and produce pain
neutrophils
inflammatory mediator that destroys bacteria but also attacks healthy cells
prostaglandins
inflammatory mediator that vasodilates and increases vascular permeability
serotonin
inflammatory mediator that promotes vasoconstriction
leukotrienes
inflammatory mediator that causes smooth muscle contraction, increases vascular permeability, and attracts neutrophils
removing debris and temporarily repairing tissue
goals of proliferation phase
72 hours post injury to 3 weeks
proliferation phase duration
resolution, regeneration, repair
types of tissue repair during the proliferation phase
finish cleaning up the area
increase strength of the repaired or replaced tissues
goals of maturation/remodeling phase
Type III
type of collagen placed in tissue regeneration of proliferation phase
Type I
collagen type placed during maturation/remodeling phase to replace Type III fibers
keys to success in maturation/remodeling phase
rehab
appropriate stress
eccentric and concentric exercises
metaplasia
dysplasia
hyperplasia
atrophy
hypertrophy
soft tissue adaptations
metaplasia
conversion of one kind of tissue to another (ex myositis ossification)