Final Exam Flashcards
1
Q
Muscular sys consists of 3 types of muscle called
A
cardiac, smooth, and skeletal
2
Q
What is the most abundant tissue in the human body?
A
skeletal muscle, and is about 40-45% of total body weight
3
Q
Skeletal muscle provides 5 things
A
Strength stability protection for the skeleton enable bones to move provide stabilization for body posture against gravity
4
Q
Skel muscles perform both
A
dynamic and static work (on test asshole)
5
Q
Sarcomere
A
structural unit of skeletal muscle, a multinucleated muscle cell or fiber
6
Q
muscle fiber thickness
A
10-100um
7
Q
muscle fiber length
A
1-30 cm
8
Q
Muscle fibers consist of
A
myofibrils
9
Q
sarcomeres in series:
A
basic contractile unit of muscle
10
Q
Myofibrils consist of myofilaments called:
A
actin, myosin, troponin, and tropomysin, and Titin/convexin
11
Q
Sarcomere composite lines
A
z line to z line ~= 1.27 - 3.6 um in length
12
Q
thin filament of sarcomere is what and size
A
actin: 5nm in diameter
13
Q
thick filaments and size
A
myosin: 15 nm in diameter
14
Q
What is the largest structure protein in the body called
A
Titin/convexin
15
Q
Titin does what? and may have what?
A
anchors myosin filament to Z-line may have crossbridge sites
16
Q
Myofilaments in parallel w/
A
sarcomere
17
Q
Sarcomeres in series within
A
myofibrils
18
Q
What is the contractile unit of the muscle cell?
A
sarcomere including the connective tissue aka the-ysiums
19
Q
What is the contractile unit of the muscle cell?
A
sarcomere including the connective tissue aka the-ysiums
20
Q
Motor Unit
A
functional unit of muscle contraction
21
Q
motor unit is composed of
A
motor neuron and all muscle cells (fibers) innervated by motor neuron
22
Q
motor unit follows what principle which is what
A
all or none principle- impulse from motor neuron will contraction in all muscle fibers it innervates or none at all
23
Q
Based on the size principle, what is recruited first?
A
the smallest motor units recruited first aka type I
24
Q
Blank are recruited with lower stimulation frequencies
A
small motor untis, doesnt take long to turn on
25
What has
g
26
final control of movement and size principle
Smallest motor units with relatively low levels of tension provide for finer control of movement such as eyes
27
Blank are recruited later with ___ frequency of stimulation and _________ need for ___________ tension
Larger motor units recruited later with increased freq of stim and increased need for greater tension to turn on
28
According to size principle, what turns off first and this could also be what to muscle and why is this asshole dick fart?
larger motor units
Tension is reduced by the reverse process due to successive reduction of firing rate and dropping off of large units first
29
According to size principle, what turns off first and this could also be what to muscle and why is this asshole dick fart?
larger motor units
Tension is reduced by the reverse process due to successive reduction of firing rate and dropping off of large units first
30
Length-tension relationship force of contraction in single fiber determined by what
overlap of actin and myosin such as alterations in sarcomere
31
Length-tension relationship force of contraction for whole muscle must
account for active (contractile) and passive (series and parallel elastic elements) components
32
What are series elastic tissues?
Tissues in series with contractile component, and tendons forms series elastic element of skeletal muscle (w/in skel muscle). This is when the endomysium, perimysium, and epimysium are continuous with connective tissue of tendon. They lengthen slightly under isometric contraction (= 3-7% of muscle length). This is a potential mechanism for stored elastic potential energy, an example of this is function in prestretch of muscle prior to explosive concentric contraction, so it is a storage site of potential energy.
33
What are series elastic tissues?
Tissues in series with contractile component, and tendons forms series elastic element of skeletal muscle (w/in skel muscle). This is when the endomysium, perimysium, and epimysium are continuous with connective tissue of tendon. They lengthen slightly under isometric contraction (= 3-7% of muscle length). This is a potential mechanism for stored elastic potential energy, an example of this is function in prestretch of muscle prior to explosive concentric contraction, so it is a storage site of potential energy
34
Musculotendinous unit
tendon and connective tissues in muscle (sarcolemma, endomysium, perimysium, and epimysium) are viscoelatic
35
Viscoelastic structures help
determine mechanical characteristics of muscles during contraction and passive extension
36
viscoelastic:
lengthening capacity of the involved structures (epi, endo, peryimysium), this protects the muscle and tendon based ROM decreases, so injuires can happen
37
viscoelastic:
lengthening capacity of the involved structures (epi, endo, peryimysium), this protects the muscle and tendon based ROM decreases, so injuires can happen
38
F(x) of elastic elements of muscle
1) Keep "ready" state for muscle contraction
2) Contribute to smooth contraction w/o contraction would be very rigid, elastic makes it smooth tissue w/ motor
3) Reduce force buildup on muscle and may prevent or reduce muscle injury
4) Viscoelastic property may help muscle absorb, store, and return energy, this where energy stored (Potential enrgy).
39
Concentric/shortening definition
force of muscle contraction is greater than resistance
40
Concentric/shortening definition
force of muscle contraction is greater than resistance
41
Concentric/shortening Work
Positive work; muscle moment and angular velocity of joint in same direction
42
Concentric/shortening Work
Positive work; muscle moment and angular velocity of joint in same direction
43
Eccentric
| Lengthening def
Force of muscle contraction
44
Eccentric
| Lengthening work
Negative work; muscle moment and angular velocity of joint in opposite direction
45
Eccentric
| Lengthening work
Negative work; muscle moment and angular velocity of joint in opposite direction
46
Isokinetic definition
Force of muscle contraction = resistance; constant angular velocity; special case is isometric contraction
47
Isokinetic work
Positive work; muscle moment and angular velocity of joint in same direction
48
Isometric def
Force of muscle contraction
49
Isometric work
No mechanical work; physiological work
50
Isometric work
No mechanical work; physiological work
51
Concentric contraction (muscle shortening) occurs when
the force of contraction is greater than the resistance (positive work)
52
Velocity of concentric contraction is
inversely related to diff btwn force of contraction and external load
53
Zero velocity occurs
(no change in muscle length) when force = R (no mech work)
54
Zero velocity occurs
(no change in muscle length) when force = R (no mech work)
55
Eccentric contraction (muscle lengthening) occurs when the
force of contraction is less than R (negative work)
56
Velocity of eccentric contraction is
directly related to the diff between force of contraction and external load
57
In isometric contractions,
greater force can be developed to maximum contractile force, with greater time
58
In isometric contractions, increased time allows
greater force generation and transmission through parallel elastic elements to the series elastic elements (tendon)
59
In isometric contractions, maximum contractile force may be generated in the
contractile component of muscle in 10msec; transmission to the tendon may take 300msec
60
In isometric contractions, maximum contractile force may be generated in the
contractile component of muscle in 10msec; transmission to the tendon may take 300msec
61
Deformation
When a force acts on an object, that object deforms (strain)
62
Deformation
When a force acts on an object, that object deforms (strain)
63
strain
the actual deformation (final length-intial length)
64
stress
load applied
65
stress
load applied
66
Elongation
Produced from tensile load (pulling)
67
Toe region
Very little force to deform tissue. The slack in the tissue, taking up the slack
68
What defines stiffness?
slope of elastic region
69
Area under curve defines
energy that can be stored
70
elastic region
return to original configuration once load is removed
71
Yield Point:
End of the elastic region. After this point the tissue will no longer immediately return to its original state once the load is removed, microtrauma occurs, and tissue healing is required.
72
Plastic region
deformation of material will be permanent, yet structure will be intact; ligament - bad, muscle = ?
73
Plastic region
deformation of material will be permanent, yet structure will be intact; ligament - bad, muscle = ?
74
Failure point
Continuation through the plasic region; material can deform no longer and failure occurs, grade III sprian
75
Load Deformation curve is useful when
determining comparative characteristics of whole structures ex) bone, tendon, cartilage, ligaments
76
Generally accepted that flexibility is essential for
improved performance, but recent studies are conflciting this and inconclusive
77
Stretching has shown to
decrease performance parameters for stength, endurance, power, joint position sense and rxn time
78
Stretching has shown to
decrease performance parameters for stength, endurance, power, joint position sense and rxn time
79
Flexibility decrease incidence of
injury, recent studies fail to find true cause and effect relationship
80
Flexibility decrease incidence of
injury, recent studies fail to find true cause and effect relationship
81
Active ROM is what kind of flexibility?
dynamic flexibility
82
Active ROM is degree to which
a joint can be moved by muscle contraction, and not necessarily a good indicator of joint stiffness or looseness cuz movement of joint has little resistance
83
Active ROM is degree to which
a joint can be moved by muscle contraction, and not necessarily a good indicator of joint stiffness or looseness cuz movement of joint has little resistance
84
Passive ROM is what kind of flexibility
static flex
85
Passive ROM degree to which a joint can be
passively moved to end pts of ROM
86
In passive ROM no what
no muscle contraction is involved
87
In passive ROM no what
no muscle contraction is involved
88
Active and Passive ROM many situations in activity when
muscle is forced beyond its normal active limits
89
Active and Passive ROM if muscle does not have
elasticity to compensate, injury to musculotendinous unit may happen
90
Strain is due to
overstretching, overexertion, and overuse of soft tissue
91
strains tend to be less severe than a
sprain
92
strain is slight trauma or unaccustomed,
repeated trauma of a minor degree
93
Strain, typically, some degree of
disruption of the musculotendinous unit initiating the inflammatory cycle
94
Strain, typically, some degree of
disruption of the musculotendinous unit initiating the inflammatory cycle
95
Sprain is a
severe stress, stretch, or tear of soft tissue
96
Sprain is what anatomical parts
Joint capsule, ligament, tendon, or muscle
97
for sprain, typcially referrring to injury to a
ligament
98
sprain is graded
first=mild
second=moderate
third= severe
99
Subluxation
an incomplete or partial disolocation that often involves secondary trauma to surrounding soft tissue
100
dislocation
displacement of a part usually the articulating bony partners within a joint such as such tissue damage, inflammation, pain, and muscle spasm (guarding)
101
Muscle/tendon rupture or tear if partial, pain is
experience in the region of the breach when the muscle is stretched or when it contracts againts resistance
102
Complete rupture/tear
The muscle does not pull against the injury, as it is no longer attached, therefore, stretching for R applied to the musculotendinous unit does not elicit pain/provocation
103
Tendinous lesions/ tendinopathy how many kinds
4
104
Tenosynovitis
inflammation of the synovial membrane covering a tendon
105
tendinitis
inflammation of the tendon (scarring/ Ca deposits residually)
106
Tenovaginitis
inflammation with thickening of a tendon sheath
107
Tendinosis
degeneration of the tendon resulting from repetive microtrauma
108
Synovitis is
inflammation of a synovial membrane, an excess of normal synovial fluid within a joint or tendon sheath derived from trauma or disease
109
Synovitis is
inflammation of a synovial membrane, an excess of normal synovial fluid within a joint or tendon sheath derived from trauma or disease
110
Hemarthrosis
Bleeding into a joint, typically from severe trauma
111
Hemarthrosis
Bleeding into a joint, typically from severe trauma
112
ganglion
ballooning of the wall of a joint capsule or tendon sheath due to trauma or rheumatoid arthritis
113
bursitis
inflamation of a bursa
114
contusion
bruising from a direct blow
| capillary rupture, bleeding, edema, and inflammatory response
115
Overuse syndromes
cumulative trauma disorders/ repetitive strain disorders.
| Repeated, submax overload and or frictional wear to a muscle or tendon resulting in inflammation and pain
116
Overuse syndromes
cumulative trauma disorders/ repetitive strain disorders.
| Repeated, submax overload and or frictional wear to a muscle or tendon resulting in inflammation and pain
117
Dysfunction is
loss of normal function of region or tissue such as adaptive shortenings of soft tissue, adhesions, muscle weakness, and any condition resulting in loss of normal mobility
118
Joint dysfunction
mech loss of normal joint play in synovial joints that causes loss of function/pain
119
jt dysfunciton precipatating factors
trauma, immobilization, disuse, aging, or a serious pathological condition
120
contracture
shortening or tightening of skin, fascia, muscle, or joint capsule that prevents normal joint mobility or flexibility of that structure
121
Adhesions
abnormal adherence of collagen fibers to surrounding structures restricting normal elasticity of the involved structures
122
Adhesion examples
immobs
following traum
surgical complication
123
Reflex Muscle Guarding
Prolonged contraction of a muscle in response to a painful stimulus, and the pain causing lesion may originate from.
124
Underlying tissue could be what condition?
Reflex muscle guarding
125
Reflex Muscle Guarding Refered pain versus not referred?
When not referred, the contracting muscle as as a splint for the injured tissue, restricting movement which would further perpetuate the inflammatory cycle
126
Guarding ceases when the
painful stimulus is relieved, theoretically
127
Intrinsic Muscle Spasm
Prolonged contraction of a muscle in response to the local circulatory and metabolic changes that occur when a muscle is in a continued state of contraction
128
Intrinsic Muscle Spasm pain results from what?
an altered circulatory/metabolic environment
129
Intrinsic Muscle Spasm the muscle contraction becomes
self perpetuating regardless of whether the primary lesion that caused the guarding state is relieved
130
Spasm
Response of a muscle to a viral infection, cold, prolonged periods of immobilization, emotional tension, direct trauma, metabolic disequilibrium, and neurological pathology
131
Spasm
Response of a muscle to a viral infection, cold, prolonged periods of immobilization, emotional tension, direct trauma, metabolic disequilibrium, and neurological pathology
132
Muscle weakness is what?
Decrease in the strength of muscle contraction due to systemic lesion/pathology, chemical source, local lesion of a nerve of the CNS/PNS, direct insult to the muscle, and inactivity
133
Grade 1 tissue severity (first deg)
Mild pain at the time of injury or within 24-48 hrs
134
Grade 1 sx
mild swelling, local tenderness, and pain when tissue is stressed
135
Grade 2 (second deg)
Moderate pain that requires stopping the activity
136
Grade 2 sx
Stress and palpation of the tissue greatly increases pain, if ligamentous origin, then some of the fibers are torn, and joint stability
137
Grade 3 (third deg)
Near complete or complete, tear or avulsion of the involved tissue (tendon or ligament) w/ severe pain
138
Grade 3 sx
Stress to the tissue is usually painless, palpation typically reveals the defect, and moderate joint instability if ligamentous/tendinous origin
139
Grade 3 sx
Stress to the tissue is usually painless, palpation typically reveals the defect, and moderate joint instability if ligamentous/tendinous origin
140
Inflammation
Any insult to connective tissue and most organ systems whether its from mechanical injury or chemical irritant, the body's responses and stages of healing are similar.
141
Duration for inflammation stages
Number of days in each stage vary, and each stage overlaps
142
What is the best guideline to determine patient response to determine exs progression?
inflammation
143
What are the stages of inflammation are there?
Acute
Subacute
Chronic-maturation
chronic-inflammation
144
Characteristics of Acute Stage Inflammation
| Cellular and humoral responses:
respond to antigens and distinguish self from non-self or damage
145
Characteristics of Acute Stage Inflammation for first 48 hrs what predominates?
vascular changes
146
What are those vascular changes in first 48hrs?
Exudation of cells and solutes from the blood vessels take place and clot formation occurs. Capillaries become more permeable with moderate exudate release in affected region, and neutralization of the chemical irrantants happen and noxius stimuli (pain) present as protective mechanism. Then, Phagocytosis cleans up the dead tissue via immune infiltration, which is edema/swelling to distend capsule and prevent normal movement. Then, early fibro-blastic activity occurs, and formation of new capillary beds to replace damaged capillaries
147
What are those vascular changes in first 48hrs?Characteristics of Acute Stage Inflammation
Exudation of cells and solutes from the blood vessels take place and clot formation occurs. Capillaries become more permeable with moderate exudate release in affected region, and neutralization of the chemical irrantants happen and noxius stimuli (pain) present as protective mechanism. Then, Phagocytosis cleans up the dead tissue via immune infiltration, which is edema/swelling to distend capsule and prevent normal movement. Then, early fibro-blastic activity occurs, and formation of new capillary beds to replace damaged capillaries
148
Characteristics of Acute Stage Inflammation duration
This stage typically last between 4-6 days, unless the insult is perpetuated
149
Clinical signs of acute stage inflammation
signs of inflammation are present including swelling/edema, redness, heat, pain, and loss of f(x), and muscle guarding and spasm (reflexive muscle contraction for regional immobs)
150
When testing ROM for acute inflammation patients what do you do mother fucker?
the individual will experience pain and there will be muscle guarding before completion of normal ROM (pain w/in normal ROM)
151
For acute inflamm, immune overrxn as per wound healing has been implicated in the devep of what disease?
cancer
152
For acute inflamm, immune overrxn as per wound healing has been implicated in the devep of what disease?
cancer
153
Subacute stage inflam characteristics
lasts and additional 10-17 days, usually, so total of 14-23 days after onset of injury, so may last up to six weeks
154
Subacute stage is characterized by the
synthesis and deposition of collagen
155
In the Subacute stage, fibroblasts are in a
tremendous number by the 4th day after the injury and this process continues in an aggressive fashion until ~ the 21st day if there are no setbacks
156
fibroblasts produce new
collagen
157
In the Subacute stage, noxious stimuli are what
removed and growth of cap beds into the new tissue takes place
158
In the Subacute stage, what activity increases
fibroblastic activity, collagen formation, and granulation of tissue development increases
159
In the Subacute stage, what activity increases
fibroblastic activity, collagen formation, and granulation of tissue development increases
160
In the Subacute stage, what replaces the exudate that originally formed the clot?
immature collagen
161
In the Subacute stage, wound closure in the muscle and skin usually take
5 - 8 days; in tendons and ligaments, 3-5 weeks
162
In the Subacute stage, proper growth and alignment can be stimulated through what?
application of appropriate tensile loading in the line of normal stress for that particular tissue
163
What is very common in the Subacute stage?
adhesion need to be minimized
164
In the Subacute stage, the clinical signs include
signs of inflamation progressively reduce and eventually appear absent
165
In the Subacute stage, when testing rom, the patient experiences what
pain synchronous upon encountering tissue resistance at the end of the available ROM
166
In the Subacute stage, when testing rom, the patient experiences what
pain synchronous upon encountering tissue resistance at the end of the available ROM
167
Chronic stage inflammation is maturation of the
connective tissue as collagen fibers from fibrils and the scar tissue matures
168
Chronic stage inflammation remolding occurs as
collagen fibers become thicker and reorient in response to stresses placed on the connective tissue, and these stresses can either be physiologically beneficial or harmful
169
Chronic stage inflammation remolding occurs as
collagen fibers become thicker and reorient in response to stresses placed on the connective tissue, and these stresses can either be physiologically beneficial or harmful
170
Chronic stage inflammation the scar begins to
retract from activity of the myofibroblasts
171
Chronic stage inflammation, the higher the density of the connective tissue, the
longer the remolding duration
172
Chronic stage inflammation, the higher the density of the connective tissue, the
longer the remodeling duration
173
Chronic stage inflammation immature collagen tissue is
bonded together via H bonds allowing adherence to surrounding tissue, they can be remolded properly via gentle and persistent treatment, and is possible for 8-10 weeks
174
Chronic remodeling if not properly stressed, the fibers
adhere to the surrounding tissues and form a restrictive scar
175
In Chronic stage inflammation, remodeling portion as the structure of collagen tissue matures, the
bonding becomes covalent, tissue thickens, becomes stronger due to the bonding conversion, and becomes more resistant to remodeling.
176
In Chronic stage inflammation, remodeling portion as the structure of collagen tissue matures, the
bonding becomes covalent, tissue thickens, becomes stronger due to the bonding conversion, and becomes more resistant to remodeling.
177
In Chronic stage inflammation, remodeling portion an old scar has a
poor response to stretch/mobilization
178
In Chronic stage inflammation, at 14 weeks, the scar tissue is
unresponsive to remodeling
179
In Chronic stage inflammation, at 14 weeks, the scar tissue is
unresponsive to remodeling
180
Clinical signs for chronic stage inflammation
there are no signs of inflammation
181
In Chronic stage inflammation, when testing ROM, the individual does not feel
pain until beyond tissue R and overpressure is applied to the appropriate structures.
182
In Chronic stage inflammation, the individual will probably demonstrate
reduced strength, decreased ROM, and some loss of f(x)
183
In Chronic stage inflammation, restoration of function begins in
this stage
184
In Chronic stage inflammation, restoration of function begins in
this stage.
185
In Chronic stage inflammation, late stages of what happens
tissue repair or recovery with no signs of inflammation yet full f(x) not regained, and chronic stage overlaps w/ the subacute stage of inflammation
186
Chronic-perpetual inflammation characteristics
If excessive stresses or irritants are applied to the developing and remodeling tissue: aggravation of the healing process ensues.
187
In the Chronic-perpetual inflammation, the inflam process is perpetuated at
low levels of intensity
188
In Chronic-perpetual inflammation, fibroblast proliferation occurs continuosly in conjunction w/
continued degradation of mature collagen; all resulting in predominance of immature, thin collagen tissue resulting in next question.
189
continued degradation of mature collagen; all resulting in predominance of immature, thin collagen tissue resulting in:
Generalized weakening of the affected tissue.
Excessive scar production
Myofibroblasts activity is perpetuated resulting in progressive limitation to functional ROM (adhesions, restricted scar tissue).
190
In Chronic-perpetual inflammation, efforts to stretch the tissue actually result in
physiological inflammation, tissue irritation, and progressive functional limits such as pain, decreased ROM and strength
191
In Chronic-perpetual inflammation, the clinical signs are
increasing pain, swellin/edema, and muscle guarding that lasts more than several hours after the activity, increased sensation of stiffness after rest w/ accompanied loss of ROM, 24 hrs after the activity, and progressive increase in stiffness due to scar tissue formation
192
In Chronic-perpetual inflammation, old scar requries
adaptive lengthening via mobs of scar and surrounding tissue or surgical release
193
In Chronic-perpetual inflammation, old scar requries
adaptive lengthening via mobs of scar and surrounding tissue or surgical release
194
Acute stage inflammation is the what phase for treatment
the protection phase of treatment
195
Acute stage inflammation treatment
Rest and protection of the injured area are necessary during the first 24 hrs, but complete immob can easily result in adherence of developing fibrils to the surrounding tissues and weakening of the connective tissue as it can't be properly remodeled
196
Acute stage inflammation treatment goals
Reduce deleterious effects of inflammation (adhesions/ contractures, etc).
Protect the region from another injury.
Prevent the degrading effects of immobility.
197
Acute stage inflammation treatment too much motion at this stage will be what and will do what
will be painful and will reinjure the tissue, so no provocation of tissues in the first 24-48 hrs (as little as possible)
198
Acute stage inflammation treatment typically passive ROM as active ROM is what
contraindicated
199
Acute stage inflammation AROM to
regional tissues that do not directly impact the injured site is optimal
200
Acute stage inflammation AROM to
regional tissues that do not directly impact the injured site is optimal
201
Acute stage inflammation treatment considerations
| control what?
control pain, edema, spasm by cold, compression, elevation, low grade tx, massage 48 hrs, limit motion via rest/protection via splinting?, avoid positions of stress, and appropriate dosage of PROM as well
202
Contraindications of acute treatment considerations
AROM
Stretching activities
Resistance exs
203
Contraindications of acute treatment considerations
AROM
Stretching activities
Resistance exs
204
subacute stage the individual often feels
good in this stage and returns to normal activity too soon
205
subacute stage criteria for exs initiation
Decreased swelling, constant pain meds, available ROM pain free both PROM AND AROM, activity must remain w/in safe dosage w/ appropriate signs; being a progressive daily reduction in pain and swelling.
206
Subacute treament
Start w/ single plane motions and progress to multi-planar motions. Constantly, re-eval the efficacy of the exs. Then begin w/ open chain exs and progress to protected closed chain exercises. Eccentric exercises will most likely reinjure the tissue in the early sub-acute stage: May be beneficial as tissues transition in chronic maturation stage. Then begin with mild tissue lengthening, and maintain function at unrelated regions of the body.
207
Chronic-remodeling stage
Primary differences between the late sub-acute stage of healing and the chronic stage of healing is the orientation of collagen fibers, so there needs to be a balance between collagen synthesis and collagen degradation.
208
Remodeling of collagen tissue depends upon the
stress placed upon the tissue so utilize controlled forces in the appropriate planes/ appropriate stresses
209
in Chronic-remodeling stage, what kinds of stresses will result in tissue reinjury and chronic inflammation?
excessive or abnormal stresses
210
Chronic-remodeling stage
Primary differences between the late sub-acute stage of healing and the chronic stage of healing is the orientation of collagen fibers, so there needs to be a balance between collagen synthesis and collagen degradation.
211
in Chronic-remodeling stage, what kinds of stresses will result in tissue reinjury and chronic inflammation?
excessive or abnormal stresses
212
In the Chronic-remodeling stage, if full ROM continues through stages of healing, and no return to acute/subacute stage inflammation happens, then what happens
then acitivity progression continues w/ greater complexity and intensity towards PLF
213
In the Chronic-remodeling stage, pain felt by the patient should only be the result of what
stress placed upon tissue adhesions or contractures beyond the normal ROM
214
contractures and adhesions require what
mobs at this stage of recovery in order to avoid a set back
215
contractures and adhesions require what
mobs at this stage of recovery in order to avoid a set back
216
Chronic stage treatment
Joint motion w/o adequate muscle support/stabilization will cause trauma to that jt as functional activities are progressed through
217
Chronic stage healing w/
progresivley increasing tensile quality in the injured tissue will continue for 12-18 m depending on the environment created through rehab
218
Chronic stage healing w/
progresivley increasing tensile quality in the injured tissue will continue for 12-18 m depending on the environment created through rehab
219
Overuse
repitive nature of the precipatiating event (microtrauma)
220
For overuse chronic recurring pain injury, initially the inflammation is what
subthreshold (not definitively detectable), but builds to levels of perceived pain and dysfunction
221
Chronic overuse results in
results in perpetual sub-acute stage of inflammation
222
Chronic overuse is characterized by
small/weak collagen fibrils (immature)
223
Trauma following
superimposed repitive trauma (overuse) results in a condition of chronic inflammation as the tissues are never allowed to heal
224
(Trauma) Premature return to high demand functional activites before
proper tissue remodeling/healing has happened
225
Trauma with Premature return to high demand functional activites before proper tissue remodeling/healing has happened results in
chronic perpetual inflammation and dysfunction (contracture, adh, weakness, scar tissue accumulation/ reduced angiogenesis)
226
Reinjury of an "old scar":
Scar tissue is not as compliant to stress as the surrounding, undamaged tissue.
227
If the scar is adhered to the surrounding tissues or is not properly remodeled to the stresses placed upon it: wat happens
Alteration in force transmission like section of frayed rope.
Alteration of energy absorption (weakened region due to inmature tissue).
The region becomes more susceptible to injury upon stresses that would not injure normal tissue.
Weak link in the chain.
228
If the scar is adhered to the surrounding tissues or is not properly remodeled to the stresses placed upon it: wat happens
Alteration in force transmission like section of frayed rope.
Alteration of energy absorption (weakened region due to inmature tissue).
The region becomes more susceptible to injury upon stresses that would not injure normal tissue.
Weak link in the chain.
229
Imbalance between length and speed in what results in what
muscles around joints results in faulty mechanics of joint motion or abnormal forces through the muscles/joints
230
Rapid or Excessive repeated eccentric demand placed on muscles prematurely when the muscle is not
remodeled adequately for that strain, and results in tissue failure at the musculotendinous region/junction and possible myofiber necrosis
231
Rapid or Excessive repeated eccentric demand placed on muscles prematurely when the muscle is not
remodeled adequately for that strain, and results in tissue failure at the musculotendinous region/junction and possible myofiber necrosis
232
Muscle weakness is inability to
respond to excessive load demands due to resultant muscle fatigue with reduced contractility and shock-absorbing capabilities, and increased stress to supporting tissues
233
Muscle weakness is inability to
respond to excessive load demands due to resultant muscle fatigue with reduced contractility and shock-absorbing capabilities, and increased stress to supporting tissues
234
Bone malalignment or poor structural support due to
poor joint mechanics of force transmission through joint (sub-talar jt) and the joints of the associated chain
235
Change in normal intensity or demands is due to
training intensity and job demands
236
Return to activity too soon after injury results in chronic inflammation cuz
tissue not mature enough for return resulting inadequate remodeling
237
Sustained deleterious postures or motions is due to
mech disadv resulting in excessive muscle fatigue, then inflam onset/delterious adapts
238
environ factors for chronic inflammsation
work station/ cold/ vibration/ inappropraite weight bearing surface
239
Aging as contrubition chronic inflammation
tissues tolerate less stress with age, typically due to lack of visitation, ,if we atempt activities that were not provactive in younger age, but are provocative inadvancing age
240
Training errors contribute to chronic inflammation
Method/intensity/ duration/ amt/ equipment/ abnormal stresses/ condition of individual
241
NSAIDs
Non-steroidal anti-inflam drugs
242
NSAIDs
Non-steroidal anti-inflam drugs
243
NSAID Properties
Anti-inflam
analgesic
antipyretic
anti-coagulation
244
antipyretic
reduce fever
245
analgesic
painkiller
246
analgesic
painkiller
247
Mainstay in the treatment of mild-moderate pain for ppl in the US is what drug
NSAIDs
248
What is the best representative NSAIDs
aspirin
249
What is the best representative NSAIDs
aspirin
250
In 1970s, aspirin was found to what
inhibit the synthesis of a group of endogenous compound known as prostaglandins
251
In 1970s, aspirin was found to what
inhibit the synthesis of a group of endogenous compound known as prostaglandins
252
aspirin chemical named
Acetylsalicyclic Acid (ASA)
253
Asprin
Most frequently used w/ widest range of therapeautic effects
254
Aspirin
Most frequently used w/ widest range of therapeautic effects and most inexpensive NSAID
255
Prostaglandins
lipid-like compounds that exhibit a multitude of physiological activites
256
Prostaglandins are synthesized by all
human cells with the exception of RBCs
257
Prostaglandins are hormones that act to
regulate cell function under both normal and pathologic conditions
258
Prostaglandins are hormones that act to
regulate cell function under both normal and pathologic conditions
259
Thromboxanes and leukotrienes are what?
hormones derived from the same precursors as prostaglandins and are involved in physiological functions
260
Prostaglandins, thromboxanes, and leukotrienes are collectively reffered to as
eicosanoids
261
Prostaglandins, thromboxanes, and leukotrienes are collectively referred to as
eicosanoids
262
Prostaglandins, thromboxanes, and leukotrienes are collectively referred to as
eicosanoids
263
eicosanoids are derived from a
20-C fatty acid typically called arachadonic acid
264
eicosanoids are derived from a
20-C fatty acid typically called arachadonic acid
265
Arachadonic acid is what in diet?
ingested in diet
266
arachadonic acid is stored in the
phospholipid component of plasma membrane
267
When needed, arachadonic acid is cleaved from the
plasma membrane via the phospholipase A enzyme
268
Of the eicosanoids, the primary biological compound generated is :
COX- cyclooxygenase enzyme
| A secondary system involves synthesis of lipoxygenase (LOX) enzyme
269
Prostaglandins and thromboxanes are syntehsised from the
COX pathways
270
Leukotrienes are derived from
LOX enzyme
271
Physiological status and type of enzyme metabolism of cell determines
pathways and derivatives
272
NSAIDs are what kind of inhbitors and not what
they are COX inhibitors (prostaglandins & thromboxanes) not LOX inhbitors
273
Any drug that inhibits COX will eliminate all what
prostaglandin and thromboxane synthesis in that cell, region, or systemically
274
Prostaglandins are what?
pro-inflammatory (why they are inhbited you dumbass)
275
Prostaglandins are what?
pro-inflammatory (why they are inhbited you dumbass)
276
Leukotrienes are?
Pro-inflam, more so tend to mediate airway inflammation in conditions such as asthma
277
Leukotrienes are?
Pro-inflam, more so tend to mediate airway inflammation in conditions such as asthma
278
Eicosanoids can influence what functions and the effects can be
cardiovascular, respiratory, renal, GI, nervous, and reproducitve f(x), and effects can be generalzied
279
PGEs and PGIs tend to produce what where?
vasodilation in most vascular beds
280
PGFs and Thromboxanes often result in
vasoconstriction
281
Cells invovled w/ injury/trauma or disturbances to homeostasis tend to
increase production of prostaglandins
282
Cells involved w/ injury/trauma or disturbances to homeostasis tend to
increase production of prostaglandins
283
eicosanoids are
protective/inflammatory response to cellular injury
284
eicosanoids and inflammation increased what
prostaglandin synthesis at site of injury
285
PGE2 mediates
the local acute inflam response
286
the local acute inflam response:
Erythema/edema
287
Erythema/edema increase
cap permeability/blood flow/ increase histamine-bradykinin
288
Eicosanoids and pain
eicos dont produce pain directly, yet increase sensitivity of pain receptors to cascade (free nerve endings/nociceptors)
289
Fever, prostaglandins are
pyretogenic, locally and at the hypothalamus
290
Thrombus formation:
Thromboxanes cause platelet aggregation resulting in blood clots
291
DVT initiated by what
abnormal thromboxane production
292
Prostaglandins have been implicated in
CV disorders such as HTN, cancer (colon), asthma, MS, and endocrine disorders (DM),
293
Prostaglandins have been implicated in
CV disorders such as HTN, cancer (colon), asthma, MS, and endocrine disorders (DM),
294
PGAs do what to vascular smooth muscle and what to GI secretions?
vasodilation
| decrease
295
PGAs do what to vascular smooth muscle and what to GI secretions?
vasodilation
| decrease
296
PGEs do what?
vasodilation, bronchodialtion, GI smooth muscle contraction, decrease GI secretions, and platelet aggregation is varriable
297
PGEs do what?
vasodilation, bronchodialtion, GI smooth muscle contraction, decrease GI secretions, and platelet aggregation is varriable
298
PGEs do what?
vasodilation, bronchodialtion, GI smooth muscle contraction, decrease GI secretions, and platelet aggregation is varriable
299
PGIs job
vasodilation, GI smooth muscle relaxation, decrease GI secretions, and decrease platelet aggregation
300
PGIs job
vasodilation, GI smooth muscle relaxation, decrease GI secretions, and decrease platelet aggregation
301
PGFs do what asshole?
varriable vascular smooth muscle, bronchoconstriction, and contraction GI smooth muscle
302
PGFs do what asshole?
varriable vascular smooth muscle, bronchoconstriction, and contraction GI smooth muscle
303
TXAs do what?
vasoconstriction, bronchoconstriction, and increase platelet aggregation
304
LTs do what
vasoconstriction, bronchoconstriction, and contraction of GI smooth muscle
305
LTs do what?
vasoconstriction, bronchoconstriction, and contraction of GI smooth muscle
306
NSAIDs MOA
Potent inhibitor of COX enzyme
| COX inhibitors
307
COX represents what?
The first step in the synthesis of prostaglandins and thromboxanes
308
COX inhibitors prevent the formation of
prostaglandins and thromboxanes by inhibiting the COX enzyme
309
Since Prostaglandins and thromboxanes are responsible for producing the cascade of pain, inflamation, fever, and excessive blood clotting, the therapeutic effects of NSAIDs can all be attributed to their ability to
inhibit cox enzyme and can eliminate the cascade
310
Since Prostaglandins and thromboxanes are responsible for producing the cascade of pain, inflamation, fever, and excessive blood clotting, the therapeutic effects of NSAIDs can all be attributed to their ability to
inhibit cox enzyme and can eliminate the cascade
311
COX-1 enzyme does what?
Physiologic prostaglandin formation in cells mediating normal cell activity and maintaining homeostasis
312
COX-1 enzyme in the stomach mucosa synthesize prostaglandins that do what asshole fuck head?
protect the lining of the stomach from gastric acid, increase stomach mucous production, and increase blood flow to stomach mucosa
313
COX-1 enzyme in the stomach mucosa synthesize prostaglandins that do what asshole fuck head?
protect the lining of the stomach from gastric acid, increase stomach mucous production, and increase blood flow to stomach mucosa
314
COX-1 in the kidneys, they maintain what?
normal renal f(x), especially when the function is compromised
315
COX-1 synthesizes prostglandins and thromboxanes that regulate
normal platelet activity
316
XO
j
317
COX-2 is produced primarily in
injured cells and produce prostaglandins that mediate pain and propagate the inflammatory cycle
318
COX-2 production results from the prescence of injury mediators; cytokines/growth factors such as
IL-6/angiogenesis
319
COX-2 are what kinds of enzymes that do what
Emergency enzymes that protect from further injury and allow healing
320
COX-3 is what kind of prostaglandin formation
CNS prostaglandin formation
321
COX-3 is what kind of prostaglandin formation
CNS prostaglandin formation
322
COX-3 functions where and not where
functions centrally not locally
323
Acetominophen seems to be selective for the
COX-3 enzyme
324
COX-3 is rationale for acetominphen's
pain reliever/ anti-pyretic effects yet will explain why it isnt anti-inflam or anti-coag
325
COX-3 is rationale for acetominphen's
pain reliever/ anti-pyretic effects yet will explain why it isnt anti-inflam or anti-coag
326
COX-1 role
cell component that synthesizes prostaglandins to help regulate and maintain normal cell activity
327
COX-1 inhibition results in
dysequilibrium of normal cellular functions
328
COX-1 inhibition results in
dysequilibrium of normal cellular functions
329
COX-2 role
emergency enzyme that often synthesizes prostaglandins in response to cell injruy
330
COX-2 inhibition results in
termination of the inflammatory cascade
331
COX-2 inhibition results in termination of the inflammatory cascade, so the cessation of the following and one hinders
```
cessation of :
fibroblastic activity
macrophage activity and phagocytosis
angiogensis
granulation of tissue formation
hinders tissue remodeling
```
332
What happens when there is a bone fracture?
ask profess
333
What happens when there is a bone fracture?
ask profess
334
What happens when there is a bone fracture?
ask profess
335
NSAIDs inhibit the synthesis of both
COX-1 and COX-2 enzymes
336
NSAIDs decrease pain and inflammation how?
by inhbiting the COX-2 enzyme
337
NSAIDs decrease pain and inflammation how?
by inhbiting the COX-2 enzyme
338
NSAIDs inhibit synthesis of the
COX-1 enzyme that eliminates the beneficial/protective effects of COX-1 enzyme
339
NSAIDs inhibit synthesis of the COX-1 enzyme that eliminates the beneficial/protective effects of COX-1 enzyme, which can result in:
gastric damage, excessive clotting, and decreased renal function
340
NSAIDs contraindicated for
antipyretic use in kids/teens w/ influenza/ chicken pox
341
Reye Syndrome
Reye syndrome is an extremely rare but serious illness that can affect the brain and liver. It's most common in kids who are recovering from a viral infection, and is linked with NSAIDs during the infection.
342
Reye Syndrome
Reye syndrome is an extremely rare but serious illness that can affect the brain and liver. It's most common in kids who are recovering from a viral infection, and is linked with NSAIDs during the infection.
343
Why do NSAIDs increase clotting?
answer this mofo
344
Why do NSAIDs increase clotting?
answer this mofo
345
NSAIDs side effects
Hepato-toxicity
Acute renal failure
inhibit bone healing after fx or surgery involving fusion bone
346
NSAIDs can cause hepato-toxicity in patients with liver disease due to
reduced blood flow and function in the liver
347
Acute renal failure is due to
reduced blood flow and function in the kidneys
348
COX-2 Selective drugs do what?
inhibit COX-2 enzyme, thereby inhbiting the inflammatory prostaglandins, yet spare the COX-1 enzymes that regulate normal functin
349
COX-2 selective drugs reduced incidence of what?
gastric irritation, yet still present
350
COX-2 selective drugs do not do what? Yet, . . . . . . .?
they dont inhibit platelet f(X), but good in cases of prolonged bleeding and ulcers, yet they impair the synthesis of prostacyclin, a prostaglandin that promotes vasodilation and prevents platelet-induced occulsion in the coronary and carotid arteries
351
COX-2 selective drugs don't inhibit the production of what
thromboxane from the COX-1 enzyme pathway, the prostaglandin that facilitates platelet aggregation and clot formation that results in coronary & carotid artery platelet aggregation and vasoconstriction
352
COX-2 selective drugs have high prevalence of what?
MI, PE, and stroke assoicated with COX-2 selective drugs , and also bronchoconstriction
353
COX-2 selective drugs have high prevalence of what?
MI, PE, and stroke assoicated with COX-2 selective drugs , and also bronchoconstriction
354
Acetaminophen equal to NSAIDs in:
analgesia and antipyretic effects
355
Acetaminophen is NO appreciable how
anti-inflammatory effects and anti-coag effects
356
Acetaminophen is NO appreciable how
anti-inflammatory effects and anti-coag effects
357
Acetaminophen is NO appreciable how
anti-inflammatory effects and anti-coag effects
358
Acetaminophen is NO appreciable how
anti-inflammatory effects and anti-coag effects
359
Acetaminophen high dose are
toxic to liver
360
Acetaminophen high dose are toxic to liver
| Acetaminophen >
N-acetyl-p-benzoquinoneimine (NAPQI) and quickly detoxified by glutathione to the product mercapteric acid which is sent to the kidneys for excretion
361
Acetaminophen high dose are toxic to liver
| Acetaminophen >
N-acetyl-p-benzoquinoneimine (NAPQI) and quickly detoxified by glutathione to the product mercapteric acid which is sent to the kidneys for excretion
362
glutathione to the product mercapteric acid which is sent to the kidneys for excretion rxn occurs sufficiently at
moderate [ ], yet at high dosages, this rxn cannot keep up and NAPQI [ ] build up to toxic levels, inducing hepatic necrosis
363
What if it is a normal dose, yet compromised liver?
Ask profess.
| The liver will not process it rgith
364
What if it is a normal dose, yet compromised liver?
Ask profess.
| The liver will not process it rgith
365
erythema
redness of the skin or mucous membranes, caused by hyperemia of superficial capillaries. It occurs with any skin injury, infection, or inflammation.
