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Medical Perspectives 411 > Final Exam > Flashcards

Final Exam Flashcards

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USMLE® Step 1 flashcards
1
Q

Muscular sys consists of 3 types of muscle called

A

cardiac, smooth, and skeletal

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2
Q

What is the most abundant tissue in the human body?

A

skeletal muscle, and is about 40-45% of total body weight

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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
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4
Q

Skel muscles perform both

A

dynamic and static work (on test asshole)

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5
Q

Sarcomere

A

structural unit of skeletal muscle, a multinucleated muscle cell or fiber

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6
Q

muscle fiber thickness

A

10-100um

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7
Q

muscle fiber length

A

1-30 cm

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8
Q

Muscle fibers consist of

A

myofibrils

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9
Q

sarcomeres in series:

A

basic contractile unit of muscle

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10
Q

Myofibrils consist of myofilaments called:

A

actin, myosin, troponin, and tropomysin, and Titin/convexin

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11
Q

Sarcomere composite lines

A

z line to z line ~= 1.27 - 3.6 um in length

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12
Q

thin filament of sarcomere is what and size

A

actin: 5nm in diameter

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13
Q

thick filaments and size

A

myosin: 15 nm in diameter

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14
Q

What is the largest structure protein in the body called

A

Titin/convexin

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15
Q

Titin does what? and may have what?

A

anchors myosin filament to Z-line may have crossbridge sites

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16
Q

Myofilaments in parallel w/

A

sarcomere

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17
Q

Sarcomeres in series within

A

myofibrils

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18
Q

What is the contractile unit of the muscle cell?

A

sarcomere including the connective tissue aka the-ysiums

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19
Q

What is the contractile unit of the muscle cell?

A

sarcomere including the connective tissue aka the-ysiums

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20
Q

Motor Unit

A

functional unit of muscle contraction

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21
Q

motor unit is composed of

A

motor neuron and all muscle cells (fibers) innervated by motor neuron

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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

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23
Q

Based on the size principle, what is recruited first?

A

the smallest motor units recruited first aka type I

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24
Q

Blank are recruited with lower stimulation frequencies

A

small motor untis, doesnt take long to turn on

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25
Q

What has

A

g

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26
Q

final control of movement and size principle

A

Smallest motor units with relatively low levels of tension provide for finer control of movement such as eyes

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27
Q

Blank are recruited later with ___ frequency of stimulation and _________ need for ___________ tension

A

Larger motor units recruited later with increased freq of stim and increased need for greater tension to turn on

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28
Q

According to size principle, what turns off first and this could also be what to muscle and why is this asshole dick fart?

A

larger motor units
Tension is reduced by the reverse process due to successive reduction of firing rate and dropping off of large units first

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29
Q

According to size principle, what turns off first and this could also be what to muscle and why is this asshole dick fart?

A

larger motor units
Tension is reduced by the reverse process due to successive reduction of firing rate and dropping off of large units first

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30
Q

Length-tension relationship force of contraction in single fiber determined by what

A

overlap of actin and myosin such as alterations in sarcomere

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31
Q

Length-tension relationship force of contraction for whole muscle must

A

account for active (contractile) and passive (series and parallel elastic elements) components

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32
Q

What are series elastic tissues?

A

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.

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33
Q

What are series elastic tissues?

A

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

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34
Q

Musculotendinous unit

A

tendon and connective tissues in muscle (sarcolemma, endomysium, perimysium, and epimysium) are viscoelatic

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35
Q

Viscoelastic structures help

A

determine mechanical characteristics of muscles during contraction and passive extension

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36
Q

viscoelastic:

A

lengthening capacity of the involved structures (epi, endo, peryimysium), this protects the muscle and tendon based ROM decreases, so injuires can happen

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37
Q

viscoelastic:

A

lengthening capacity of the involved structures (epi, endo, peryimysium), this protects the muscle and tendon based ROM decreases, so injuires can happen

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38
Q

F(x) of elastic elements of muscle

A

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).

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39
Q

Concentric/shortening definition

A

force of muscle contraction is greater than resistance

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40
Q

Concentric/shortening definition

A

force of muscle contraction is greater than resistance

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41
Q

Concentric/shortening Work

A

Positive work; muscle moment and angular velocity of joint in same direction

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42
Q

Concentric/shortening Work

A

Positive work; muscle moment and angular velocity of joint in same direction

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43
Q

Eccentric

Lengthening def

A

Force of muscle contraction

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44
Q

Eccentric

Lengthening work

A

Negative work; muscle moment and angular velocity of joint in opposite direction

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45
Q

Eccentric

Lengthening work

A

Negative work; muscle moment and angular velocity of joint in opposite direction

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46
Q

Isokinetic definition

A

Force of muscle contraction = resistance; constant angular velocity; special case is isometric contraction

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47
Q

Isokinetic work

A

Positive work; muscle moment and angular velocity of joint in same direction

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48
Q

Isometric def

A

Force of muscle contraction

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49
Q

Isometric work

A

No mechanical work; physiological work

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50
Q

Isometric work

A

No mechanical work; physiological work

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51
Q

Concentric contraction (muscle shortening) occurs when

A

the force of contraction is greater than the resistance (positive work)

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52
Q

Velocity of concentric contraction is

A

inversely related to diff btwn force of contraction and external load

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53
Q

Zero velocity occurs

A

(no change in muscle length) when force = R (no mech work)

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54
Q

Zero velocity occurs

A

(no change in muscle length) when force = R (no mech work)

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55
Q

Eccentric contraction (muscle lengthening) occurs when the

A

force of contraction is less than R (negative work)

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56
Q

Velocity of eccentric contraction is

A

directly related to the diff between force of contraction and external load

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57
Q

In isometric contractions,

A

greater force can be developed to maximum contractile force, with greater time

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58
Q

In isometric contractions, increased time allows

A

greater force generation and transmission through parallel elastic elements to the series elastic elements (tendon)

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59
Q

In isometric contractions, maximum contractile force may be generated in the

A

contractile component of muscle in 10msec; transmission to the tendon may take 300msec

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60
Q

In isometric contractions, maximum contractile force may be generated in the

A

contractile component of muscle in 10msec; transmission to the tendon may take 300msec

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61
Q

Deformation

A

When a force acts on an object, that object deforms (strain)

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62
Q

Deformation

A

When a force acts on an object, that object deforms (strain)

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63
Q

strain

A

the actual deformation (final length-intial length)

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64
Q

stress

A

load applied

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65
Q

stress

A

load applied

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66
Q

Elongation

A

Produced from tensile load (pulling)

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67
Q

Toe region

A

Very little force to deform tissue. The slack in the tissue, taking up the slack

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68
Q

What defines stiffness?

A

slope of elastic region

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69
Q

Area under curve defines

A

energy that can be stored

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70
Q

elastic region

A

return to original configuration once load is removed

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71
Q

Yield Point:

A

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.

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72
Q

Plastic region

A

deformation of material will be permanent, yet structure will be intact; ligament - bad, muscle = ?

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73
Q

Plastic region

A

deformation of material will be permanent, yet structure will be intact; ligament - bad, muscle = ?

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74
Q

Failure point

A

Continuation through the plasic region; material can deform no longer and failure occurs, grade III sprian

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75
Q

Load Deformation curve is useful when

A

determining comparative characteristics of whole structures ex) bone, tendon, cartilage, ligaments

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76
Q

Generally accepted that flexibility is essential for

A

improved performance, but recent studies are conflciting this and inconclusive

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77
Q

Stretching has shown to

A

decrease performance parameters for stength, endurance, power, joint position sense and rxn time

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78
Q

Stretching has shown to

A

decrease performance parameters for stength, endurance, power, joint position sense and rxn time

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79
Q

Flexibility decrease incidence of

A

injury, recent studies fail to find true cause and effect relationship

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80
Q

Flexibility decrease incidence of

A

injury, recent studies fail to find true cause and effect relationship

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81
Q

Active ROM is what kind of flexibility?

A

dynamic flexibility

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82
Q

Active ROM is degree to which

A

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

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83
Q

Active ROM is degree to which

A

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

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84
Q

Passive ROM is what kind of flexibility

A

static flex

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85
Q

Passive ROM degree to which a joint can be

A

passively moved to end pts of ROM

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86
Q

In passive ROM no what

A

no muscle contraction is involved

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87
Q

In passive ROM no what

A

no muscle contraction is involved

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88
Q

Active and Passive ROM many situations in activity when

A

muscle is forced beyond its normal active limits

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89
Q

Active and Passive ROM if muscle does not have

A

elasticity to compensate, injury to musculotendinous unit may happen

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90
Q

Strain is due to

A

overstretching, overexertion, and overuse of soft tissue

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91
Q

strains tend to be less severe than a

A

sprain

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92
Q

strain is slight trauma or unaccustomed,

A

repeated trauma of a minor degree

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93
Q

Strain, typically, some degree of

A

disruption of the musculotendinous unit initiating the inflammatory cycle

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94
Q

Strain, typically, some degree of

A

disruption of the musculotendinous unit initiating the inflammatory cycle

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95
Q

Sprain is a

A

severe stress, stretch, or tear of soft tissue

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96
Q

Sprain is what anatomical parts

A

Joint capsule, ligament, tendon, or muscle

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97
Q

for sprain, typcially referrring to injury to a

A

ligament

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98
Q

sprain is graded

A

first=mild
second=moderate
third= severe

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99
Q

Subluxation

A

an incomplete or partial disolocation that often involves secondary trauma to surrounding soft tissue

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100
Q

dislocation

A

displacement of a part usually the articulating bony partners within a joint such as such tissue damage, inflammation, pain, and muscle spasm (guarding)

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101
Q

Muscle/tendon rupture or tear if partial, pain is

A

experience in the region of the breach when the muscle is stretched or when it contracts againts resistance

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102
Q

Complete rupture/tear

A

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

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103
Q

Tendinous lesions/ tendinopathy how many kinds

A

4

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104
Q

Tenosynovitis

A

inflammation of the synovial membrane covering a tendon

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105
Q

tendinitis

A

inflammation of the tendon (scarring/ Ca deposits residually)

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106
Q

Tenovaginitis

A

inflammation with thickening of a tendon sheath

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107
Q

Tendinosis

A

degeneration of the tendon resulting from repetive microtrauma

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108
Q

Synovitis is

A

inflammation of a synovial membrane, an excess of normal synovial fluid within a joint or tendon sheath derived from trauma or disease

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109
Q

Synovitis is

A

inflammation of a synovial membrane, an excess of normal synovial fluid within a joint or tendon sheath derived from trauma or disease

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110
Q

Hemarthrosis

A

Bleeding into a joint, typically from severe trauma

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111
Q

Hemarthrosis

A

Bleeding into a joint, typically from severe trauma

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112
Q

ganglion

A

ballooning of the wall of a joint capsule or tendon sheath due to trauma or rheumatoid arthritis

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113
Q

bursitis

A

inflamation of a bursa

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114
Q

contusion

A

bruising from a direct blow

capillary rupture, bleeding, edema, and inflammatory response

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115
Q

Overuse syndromes

A

cumulative trauma disorders/ repetitive strain disorders.

Repeated, submax overload and or frictional wear to a muscle or tendon resulting in inflammation and pain

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116
Q

Overuse syndromes

A

cumulative trauma disorders/ repetitive strain disorders.

Repeated, submax overload and or frictional wear to a muscle or tendon resulting in inflammation and pain

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117
Q

Dysfunction is

A

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

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118
Q

Joint dysfunction

A

mech loss of normal joint play in synovial joints that causes loss of function/pain

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119
Q

jt dysfunciton precipatating factors

A

trauma, immobilization, disuse, aging, or a serious pathological condition

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120
Q

contracture

A

shortening or tightening of skin, fascia, muscle, or joint capsule that prevents normal joint mobility or flexibility of that structure

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121
Q

Adhesions

A

abnormal adherence of collagen fibers to surrounding structures restricting normal elasticity of the involved structures

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122
Q

Adhesion examples

A

immobs
following traum
surgical complication

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123
Q

Reflex Muscle Guarding

A

Prolonged contraction of a muscle in response to a painful stimulus, and the pain causing lesion may originate from.

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124
Q

Underlying tissue could be what condition?

A

Reflex muscle guarding

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125
Q

Reflex Muscle Guarding Refered pain versus not referred?

A

When not referred, the contracting muscle as as a splint for the injured tissue, restricting movement which would further perpetuate the inflammatory cycle

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126
Q

Guarding ceases when the

A

painful stimulus is relieved, theoretically

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127
Q

Intrinsic Muscle Spasm

A

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

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128
Q

Intrinsic Muscle Spasm pain results from what?

A

an altered circulatory/metabolic environment

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129
Q

Intrinsic Muscle Spasm the muscle contraction becomes

A

self perpetuating regardless of whether the primary lesion that caused the guarding state is relieved

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130
Q

Spasm

A

Response of a muscle to a viral infection, cold, prolonged periods of immobilization, emotional tension, direct trauma, metabolic disequilibrium, and neurological pathology

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131
Q

Spasm

A

Response of a muscle to a viral infection, cold, prolonged periods of immobilization, emotional tension, direct trauma, metabolic disequilibrium, and neurological pathology

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132
Q

Muscle weakness is what?

A

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

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133
Q

Grade 1 tissue severity (first deg)

A

Mild pain at the time of injury or within 24-48 hrs

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134
Q

Grade 1 sx

A

mild swelling, local tenderness, and pain when tissue is stressed

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135
Q

Grade 2 (second deg)

A

Moderate pain that requires stopping the activity

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136
Q

Grade 2 sx

A

Stress and palpation of the tissue greatly increases pain, if ligamentous origin, then some of the fibers are torn, and joint stability

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137
Q

Grade 3 (third deg)

A

Near complete or complete, tear or avulsion of the involved tissue (tendon or ligament) w/ severe pain

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138
Q

Grade 3 sx

A

Stress to the tissue is usually painless, palpation typically reveals the defect, and moderate joint instability if ligamentous/tendinous origin

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139
Q

Grade 3 sx

A

Stress to the tissue is usually painless, palpation typically reveals the defect, and moderate joint instability if ligamentous/tendinous origin

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140
Q

Inflammation

A

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.

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141
Q

Duration for inflammation stages

A

Number of days in each stage vary, and each stage overlaps

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142
Q

What is the best guideline to determine patient response to determine exs progression?

A

inflammation

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143
Q

What are the stages of inflammation are there?

A

Acute
Subacute
Chronic-maturation
chronic-inflammation

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144
Q

Characteristics of Acute Stage Inflammation

Cellular and humoral responses:

A

respond to antigens and distinguish self from non-self or damage

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145
Q

Characteristics of Acute Stage Inflammation for first 48 hrs what predominates?

A

vascular changes

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146
Q

What are those vascular changes in first 48hrs?

A

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

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147
Q

What are those vascular changes in first 48hrs?Characteristics of Acute Stage Inflammation

A

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
Q

Characteristics of Acute Stage Inflammation duration

A

This stage typically last between 4-6 days, unless the insult is perpetuated

149
Q

Clinical signs of acute stage inflammation

A

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
Q

When testing ROM for acute inflammation patients what do you do mother fucker?

A

the individual will experience pain and there will be muscle guarding before completion of normal ROM (pain w/in normal ROM)

151
Q

For acute inflamm, immune overrxn as per wound healing has been implicated in the devep of what disease?

A

cancer

152
Q

For acute inflamm, immune overrxn as per wound healing has been implicated in the devep of what disease?

A

cancer

153
Q

Subacute stage inflam characteristics

A

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
Q

Subacute stage is characterized by the

A

synthesis and deposition of collagen

155
Q

In the Subacute stage, fibroblasts are in a

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
Q

fibroblasts produce new

A

collagen

157
Q

In the Subacute stage, noxious stimuli are what

A

removed and growth of cap beds into the new tissue takes place

158
Q

In the Subacute stage, what activity increases

A

fibroblastic activity, collagen formation, and granulation of tissue development increases

159
Q

In the Subacute stage, what activity increases

A

fibroblastic activity, collagen formation, and granulation of tissue development increases

160
Q

In the Subacute stage, what replaces the exudate that originally formed the clot?

A

immature collagen

161
Q

In the Subacute stage, wound closure in the muscle and skin usually take

A

5 - 8 days; in tendons and ligaments, 3-5 weeks

162
Q

In the Subacute stage, proper growth and alignment can be stimulated through what?

A

application of appropriate tensile loading in the line of normal stress for that particular tissue

163
Q

What is very common in the Subacute stage?

A

adhesion need to be minimized

164
Q

In the Subacute stage, the clinical signs include

A

signs of inflamation progressively reduce and eventually appear absent

165
Q

In the Subacute stage, when testing rom, the patient experiences what

A

pain synchronous upon encountering tissue resistance at the end of the available ROM

166
Q

In the Subacute stage, when testing rom, the patient experiences what

A

pain synchronous upon encountering tissue resistance at the end of the available ROM

167
Q

Chronic stage inflammation is maturation of the

A

connective tissue as collagen fibers from fibrils and the scar tissue matures

168
Q

Chronic stage inflammation remolding occurs as

A

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
Q

Chronic stage inflammation remolding occurs as

A

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
Q

Chronic stage inflammation the scar begins to

A

retract from activity of the myofibroblasts

171
Q

Chronic stage inflammation, the higher the density of the connective tissue, the

A

longer the remolding duration

172
Q

Chronic stage inflammation, the higher the density of the connective tissue, the

A

longer the remodeling duration

173
Q

Chronic stage inflammation immature collagen tissue is

A

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
Q

Chronic remodeling if not properly stressed, the fibers

A

adhere to the surrounding tissues and form a restrictive scar

175
Q

In Chronic stage inflammation, remodeling portion as the structure of collagen tissue matures, the

A

bonding becomes covalent, tissue thickens, becomes stronger due to the bonding conversion, and becomes more resistant to remodeling.

176
Q

In Chronic stage inflammation, remodeling portion as the structure of collagen tissue matures, the

A

bonding becomes covalent, tissue thickens, becomes stronger due to the bonding conversion, and becomes more resistant to remodeling.

177
Q

In Chronic stage inflammation, remodeling portion an old scar has a

A

poor response to stretch/mobilization

178
Q

In Chronic stage inflammation, at 14 weeks, the scar tissue is

A

unresponsive to remodeling

179
Q

In Chronic stage inflammation, at 14 weeks, the scar tissue is

A

unresponsive to remodeling

180
Q

Clinical signs for chronic stage inflammation

A

there are no signs of inflammation

181
Q

In Chronic stage inflammation, when testing ROM, the individual does not feel

A

pain until beyond tissue R and overpressure is applied to the appropriate structures.

182
Q

In Chronic stage inflammation, the individual will probably demonstrate

A

reduced strength, decreased ROM, and some loss of f(x)

183
Q

In Chronic stage inflammation, restoration of function begins in

A

this stage

184
Q

In Chronic stage inflammation, restoration of function begins in

A

this stage.

185
Q

In Chronic stage inflammation, late stages of what happens

A

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
Q

Chronic-perpetual inflammation characteristics

A

If excessive stresses or irritants are applied to the developing and remodeling tissue: aggravation of the healing process ensues.

187
Q

In the Chronic-perpetual inflammation, the inflam process is perpetuated at

A

low levels of intensity

188
Q

In Chronic-perpetual inflammation, fibroblast proliferation occurs continuosly in conjunction w/

A

continued degradation of mature collagen; all resulting in predominance of immature, thin collagen tissue resulting in next question.

189
Q

continued degradation of mature collagen; all resulting in predominance of immature, thin collagen tissue resulting in:

A

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
Q

In Chronic-perpetual inflammation, efforts to stretch the tissue actually result in

A

physiological inflammation, tissue irritation, and progressive functional limits such as pain, decreased ROM and strength

191
Q

In Chronic-perpetual inflammation, the clinical signs are

A

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
Q

In Chronic-perpetual inflammation, old scar requries

A

adaptive lengthening via mobs of scar and surrounding tissue or surgical release

193
Q

In Chronic-perpetual inflammation, old scar requries

A

adaptive lengthening via mobs of scar and surrounding tissue or surgical release

194
Q

Acute stage inflammation is the what phase for treatment

A

the protection phase of treatment

195
Q

Acute stage inflammation treatment

A

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
Q

Acute stage inflammation treatment goals

A

Reduce deleterious effects of inflammation (adhesions/ contractures, etc).
Protect the region from another injury.
Prevent the degrading effects of immobility.

197
Q

Acute stage inflammation treatment too much motion at this stage will be what and will do what

A

will be painful and will reinjure the tissue, so no provocation of tissues in the first 24-48 hrs (as little as possible)

198
Q

Acute stage inflammation treatment typically passive ROM as active ROM is what

A

contraindicated

199
Q

Acute stage inflammation AROM to

A

regional tissues that do not directly impact the injured site is optimal

200
Q

Acute stage inflammation AROM to

A

regional tissues that do not directly impact the injured site is optimal

201
Q

Acute stage inflammation treatment considerations

control what?

A

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
Q

Contraindications of acute treatment considerations

A

AROM
Stretching activities
Resistance exs

203
Q

Contraindications of acute treatment considerations

A

AROM
Stretching activities
Resistance exs

204
Q

subacute stage the individual often feels

A

good in this stage and returns to normal activity too soon

205
Q

subacute stage criteria for exs initiation

A

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
Q

Subacute treament

A

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
Q

Chronic-remodeling stage

A

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
Q

Remodeling of collagen tissue depends upon the

A

stress placed upon the tissue so utilize controlled forces in the appropriate planes/ appropriate stresses

209
Q

in Chronic-remodeling stage, what kinds of stresses will result in tissue reinjury and chronic inflammation?

A

excessive or abnormal stresses

210
Q

Chronic-remodeling stage

A

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
Q

in Chronic-remodeling stage, what kinds of stresses will result in tissue reinjury and chronic inflammation?

A

excessive or abnormal stresses

212
Q

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

A

then acitivity progression continues w/ greater complexity and intensity towards PLF

213
Q

In the Chronic-remodeling stage, pain felt by the patient should only be the result of what

A

stress placed upon tissue adhesions or contractures beyond the normal ROM

214
Q

contractures and adhesions require what

A

mobs at this stage of recovery in order to avoid a set back

215
Q

contractures and adhesions require what

A

mobs at this stage of recovery in order to avoid a set back

216
Q

Chronic stage treatment

A

Joint motion w/o adequate muscle support/stabilization will cause trauma to that jt as functional activities are progressed through

217
Q

Chronic stage healing w/

A

progresivley increasing tensile quality in the injured tissue will continue for 12-18 m depending on the environment created through rehab

218
Q

Chronic stage healing w/

A

progresivley increasing tensile quality in the injured tissue will continue for 12-18 m depending on the environment created through rehab

219
Q

Overuse

A

repitive nature of the precipatiating event (microtrauma)

220
Q

For overuse chronic recurring pain injury, initially the inflammation is what

A

subthreshold (not definitively detectable), but builds to levels of perceived pain and dysfunction

221
Q

Chronic overuse results in

A

results in perpetual sub-acute stage of inflammation

222
Q

Chronic overuse is characterized by

A

small/weak collagen fibrils (immature)

223
Q

Trauma following

A

superimposed repitive trauma (overuse) results in a condition of chronic inflammation as the tissues are never allowed to heal

224
Q

(Trauma) Premature return to high demand functional activites before

A

proper tissue remodeling/healing has happened

225
Q

Trauma with Premature return to high demand functional activites before proper tissue remodeling/healing has happened results in

A

chronic perpetual inflammation and dysfunction (contracture, adh, weakness, scar tissue accumulation/ reduced angiogenesis)

226
Q

Reinjury of an “old scar”:

A

Scar tissue is not as compliant to stress as the surrounding, undamaged tissue.

227
Q

If the scar is adhered to the surrounding tissues or is not properly remodeled to the stresses placed upon it: wat happens

A

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
Q

If the scar is adhered to the surrounding tissues or is not properly remodeled to the stresses placed upon it: wat happens

A

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
Q

Imbalance between length and speed in what results in what

A

muscles around joints results in faulty mechanics of joint motion or abnormal forces through the muscles/joints

230
Q

Rapid or Excessive repeated eccentric demand placed on muscles prematurely when the muscle is not

A

remodeled adequately for that strain, and results in tissue failure at the musculotendinous region/junction and possible myofiber necrosis

231
Q

Rapid or Excessive repeated eccentric demand placed on muscles prematurely when the muscle is not

A

remodeled adequately for that strain, and results in tissue failure at the musculotendinous region/junction and possible myofiber necrosis

232
Q

Muscle weakness is inability to

A

respond to excessive load demands due to resultant muscle fatigue with reduced contractility and shock-absorbing capabilities, and increased stress to supporting tissues

233
Q

Muscle weakness is inability to

A

respond to excessive load demands due to resultant muscle fatigue with reduced contractility and shock-absorbing capabilities, and increased stress to supporting tissues

234
Q

Bone malalignment or poor structural support due to

A

poor joint mechanics of force transmission through joint (sub-talar jt) and the joints of the associated chain

235
Q

Change in normal intensity or demands is due to

A

training intensity and job demands

236
Q

Return to activity too soon after injury results in chronic inflammation cuz

A

tissue not mature enough for return resulting inadequate remodeling

237
Q

Sustained deleterious postures or motions is due to

A

mech disadv resulting in excessive muscle fatigue, then inflam onset/delterious adapts

238
Q

environ factors for chronic inflammsation

A

work station/ cold/ vibration/ inappropraite weight bearing surface

239
Q

Aging as contrubition chronic inflammation

A

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
Q

Training errors contribute to chronic inflammation

A

Method/intensity/ duration/ amt/ equipment/ abnormal stresses/ condition of individual

241
Q

NSAIDs

A

Non-steroidal anti-inflam drugs

242
Q

NSAIDs

A

Non-steroidal anti-inflam drugs

243
Q

NSAID Properties

A

Anti-inflam
analgesic
antipyretic
anti-coagulation

244
Q

antipyretic

A

reduce fever

245
Q

analgesic

A

painkiller

246
Q

analgesic

A

painkiller

247
Q

Mainstay in the treatment of mild-moderate pain for ppl in the US is what drug

A

NSAIDs

248
Q

What is the best representative NSAIDs

A

aspirin

249
Q

What is the best representative NSAIDs

A

aspirin

250
Q

In 1970s, aspirin was found to what

A

inhibit the synthesis of a group of endogenous compound known as prostaglandins

251
Q

In 1970s, aspirin was found to what

A

inhibit the synthesis of a group of endogenous compound known as prostaglandins

252
Q

aspirin chemical named

A

Acetylsalicyclic Acid (ASA)

253
Q

Asprin

A

Most frequently used w/ widest range of therapeautic effects

254
Q

Aspirin

A

Most frequently used w/ widest range of therapeautic effects and most inexpensive NSAID

255
Q

Prostaglandins

A

lipid-like compounds that exhibit a multitude of physiological activites

256
Q

Prostaglandins are synthesized by all

A

human cells with the exception of RBCs

257
Q

Prostaglandins are hormones that act to

A

regulate cell function under both normal and pathologic conditions

258
Q

Prostaglandins are hormones that act to

A

regulate cell function under both normal and pathologic conditions

259
Q

Thromboxanes and leukotrienes are what?

A

hormones derived from the same precursors as prostaglandins and are involved in physiological functions

260
Q

Prostaglandins, thromboxanes, and leukotrienes are collectively reffered to as

A

eicosanoids

261
Q

Prostaglandins, thromboxanes, and leukotrienes are collectively referred to as

A

eicosanoids

262
Q

Prostaglandins, thromboxanes, and leukotrienes are collectively referred to as

A

eicosanoids

263
Q

eicosanoids are derived from a

A

20-C fatty acid typically called arachadonic acid

264
Q

eicosanoids are derived from a

A

20-C fatty acid typically called arachadonic acid

265
Q

Arachadonic acid is what in diet?

A

ingested in diet

266
Q

arachadonic acid is stored in the

A

phospholipid component of plasma membrane

267
Q

When needed, arachadonic acid is cleaved from the

A

plasma membrane via the phospholipase A enzyme

268
Q

Of the eicosanoids, the primary biological compound generated is :

A

COX- cyclooxygenase enzyme

A secondary system involves synthesis of lipoxygenase (LOX) enzyme

269
Q

Prostaglandins and thromboxanes are syntehsised from the

A

COX pathways

270
Q

Leukotrienes are derived from

A

LOX enzyme

271
Q

Physiological status and type of enzyme metabolism of cell determines

A

pathways and derivatives

272
Q

NSAIDs are what kind of inhbitors and not what

A

they are COX inhibitors (prostaglandins & thromboxanes) not LOX inhbitors

273
Q

Any drug that inhibits COX will eliminate all what

A

prostaglandin and thromboxane synthesis in that cell, region, or systemically

274
Q

Prostaglandins are what?

A

pro-inflammatory (why they are inhbited you dumbass)

275
Q

Prostaglandins are what?

A

pro-inflammatory (why they are inhbited you dumbass)

276
Q

Leukotrienes are?

A

Pro-inflam, more so tend to mediate airway inflammation in conditions such as asthma

277
Q

Leukotrienes are?

A

Pro-inflam, more so tend to mediate airway inflammation in conditions such as asthma

278
Q

Eicosanoids can influence what functions and the effects can be

A

cardiovascular, respiratory, renal, GI, nervous, and reproducitve f(x), and effects can be generalzied

279
Q

PGEs and PGIs tend to produce what where?

A

vasodilation in most vascular beds

280
Q

PGFs and Thromboxanes often result in

A

vasoconstriction

281
Q

Cells invovled w/ injury/trauma or disturbances to homeostasis tend to

A

increase production of prostaglandins

282
Q

Cells involved w/ injury/trauma or disturbances to homeostasis tend to

A

increase production of prostaglandins

283
Q

eicosanoids are

A

protective/inflammatory response to cellular injury

284
Q

eicosanoids and inflammation increased what

A

prostaglandin synthesis at site of injury

285
Q

PGE2 mediates

A

the local acute inflam response

286
Q

the local acute inflam response:

A

Erythema/edema

287
Q

Erythema/edema increase

A

cap permeability/blood flow/ increase histamine-bradykinin

288
Q

Eicosanoids and pain

A

eicos dont produce pain directly, yet increase sensitivity of pain receptors to cascade (free nerve endings/nociceptors)

289
Q

Fever, prostaglandins are

A

pyretogenic, locally and at the hypothalamus

290
Q

Thrombus formation:

A

Thromboxanes cause platelet aggregation resulting in blood clots

291
Q

DVT initiated by what

A

abnormal thromboxane production

292
Q

Prostaglandins have been implicated in

A

CV disorders such as HTN, cancer (colon), asthma, MS, and endocrine disorders (DM),

293
Q

Prostaglandins have been implicated in

A

CV disorders such as HTN, cancer (colon), asthma, MS, and endocrine disorders (DM),

294
Q

PGAs do what to vascular smooth muscle and what to GI secretions?

A

vasodilation

decrease

295
Q

PGAs do what to vascular smooth muscle and what to GI secretions?

A

vasodilation

decrease

296
Q

PGEs do what?

A

vasodilation, bronchodialtion, GI smooth muscle contraction, decrease GI secretions, and platelet aggregation is varriable

297
Q

PGEs do what?

A

vasodilation, bronchodialtion, GI smooth muscle contraction, decrease GI secretions, and platelet aggregation is varriable

298
Q

PGEs do what?

A

vasodilation, bronchodialtion, GI smooth muscle contraction, decrease GI secretions, and platelet aggregation is varriable

299
Q

PGIs job

A

vasodilation, GI smooth muscle relaxation, decrease GI secretions, and decrease platelet aggregation

300
Q

PGIs job

A

vasodilation, GI smooth muscle relaxation, decrease GI secretions, and decrease platelet aggregation

301
Q

PGFs do what asshole?

A

varriable vascular smooth muscle, bronchoconstriction, and contraction GI smooth muscle

302
Q

PGFs do what asshole?

A

varriable vascular smooth muscle, bronchoconstriction, and contraction GI smooth muscle

303
Q

TXAs do what?

A

vasoconstriction, bronchoconstriction, and increase platelet aggregation

304
Q

LTs do what

A

vasoconstriction, bronchoconstriction, and contraction of GI smooth muscle

305
Q

LTs do what?

A

vasoconstriction, bronchoconstriction, and contraction of GI smooth muscle

306
Q

NSAIDs MOA

A

Potent inhibitor of COX enzyme

COX inhibitors

307
Q

COX represents what?

A

The first step in the synthesis of prostaglandins and thromboxanes

308
Q

COX inhibitors prevent the formation of

A

prostaglandins and thromboxanes by inhibiting the COX enzyme

309
Q

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

A

inhibit cox enzyme and can eliminate the cascade

310
Q

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

A

inhibit cox enzyme and can eliminate the cascade

311
Q

COX-1 enzyme does what?

A

Physiologic prostaglandin formation in cells mediating normal cell activity and maintaining homeostasis

312
Q

COX-1 enzyme in the stomach mucosa synthesize prostaglandins that do what asshole fuck head?

A

protect the lining of the stomach from gastric acid, increase stomach mucous production, and increase blood flow to stomach mucosa

313
Q

COX-1 enzyme in the stomach mucosa synthesize prostaglandins that do what asshole fuck head?

A

protect the lining of the stomach from gastric acid, increase stomach mucous production, and increase blood flow to stomach mucosa

314
Q

COX-1 in the kidneys, they maintain what?

A

normal renal f(x), especially when the function is compromised

315
Q

COX-1 synthesizes prostglandins and thromboxanes that regulate

A

normal platelet activity

316
Q

XO

A

j

317
Q

COX-2 is produced primarily in

A

injured cells and produce prostaglandins that mediate pain and propagate the inflammatory cycle

318
Q

COX-2 production results from the prescence of injury mediators; cytokines/growth factors such as

A

IL-6/angiogenesis

319
Q

COX-2 are what kinds of enzymes that do what

A

Emergency enzymes that protect from further injury and allow healing

320
Q

COX-3 is what kind of prostaglandin formation

A

CNS prostaglandin formation

321
Q

COX-3 is what kind of prostaglandin formation

A

CNS prostaglandin formation

322
Q

COX-3 functions where and not where

A

functions centrally not locally

323
Q

Acetominophen seems to be selective for the

A

COX-3 enzyme

324
Q

COX-3 is rationale for acetominphen’s

A

pain reliever/ anti-pyretic effects yet will explain why it isnt anti-inflam or anti-coag

325
Q

COX-3 is rationale for acetominphen’s

A

pain reliever/ anti-pyretic effects yet will explain why it isnt anti-inflam or anti-coag

326
Q

COX-1 role

A

cell component that synthesizes prostaglandins to help regulate and maintain normal cell activity

327
Q

COX-1 inhibition results in

A

dysequilibrium of normal cellular functions

328
Q

COX-1 inhibition results in

A

dysequilibrium of normal cellular functions

329
Q

COX-2 role

A

emergency enzyme that often synthesizes prostaglandins in response to cell injruy

330
Q

COX-2 inhibition results in

A

termination of the inflammatory cascade

331
Q

COX-2 inhibition results in termination of the inflammatory cascade, so the cessation of the following and one hinders

A 
cessation of :
fibroblastic activity
macrophage activity and phagocytosis
angiogensis
granulation of tissue formation
hinders tissue remodeling
332
Q

What happens when there is a bone fracture?

A

ask profess

333
Q

What happens when there is a bone fracture?

A

ask profess

334
Q

What happens when there is a bone fracture?

A

ask profess

335
Q

NSAIDs inhibit the synthesis of both

A

COX-1 and COX-2 enzymes

336
Q

NSAIDs decrease pain and inflammation how?

A

by inhbiting the COX-2 enzyme

337
Q

NSAIDs decrease pain and inflammation how?

A

by inhbiting the COX-2 enzyme

338
Q

NSAIDs inhibit synthesis of the

A

COX-1 enzyme that eliminates the beneficial/protective effects of COX-1 enzyme

339
Q

NSAIDs inhibit synthesis of the COX-1 enzyme that eliminates the beneficial/protective effects of COX-1 enzyme, which can result in:

A

gastric damage, excessive clotting, and decreased renal function

340
Q

NSAIDs contraindicated for

A

antipyretic use in kids/teens w/ influenza/ chicken pox

341
Q

Reye Syndrome

A

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
Q

Reye Syndrome

A

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
Q

Why do NSAIDs increase clotting?

A

answer this mofo

344
Q

Why do NSAIDs increase clotting?

A

answer this mofo

345
Q

NSAIDs side effects

A

Hepato-toxicity
Acute renal failure
inhibit bone healing after fx or surgery involving fusion bone

346
Q

NSAIDs can cause hepato-toxicity in patients with liver disease due to

A

reduced blood flow and function in the liver

347
Q

Acute renal failure is due to

A

reduced blood flow and function in the kidneys

348
Q

COX-2 Selective drugs do what?

A

inhibit COX-2 enzyme, thereby inhbiting the inflammatory prostaglandins, yet spare the COX-1 enzymes that regulate normal functin

349
Q

COX-2 selective drugs reduced incidence of what?

A

gastric irritation, yet still present

350
Q

COX-2 selective drugs do not do what? Yet, . . . . . . .?

A

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
Q

COX-2 selective drugs don’t inhibit the production of what

A

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
Q

COX-2 selective drugs have high prevalence of what?

A

MI, PE, and stroke assoicated with COX-2 selective drugs , and also bronchoconstriction

353
Q

COX-2 selective drugs have high prevalence of what?

A

MI, PE, and stroke assoicated with COX-2 selective drugs , and also bronchoconstriction

354
Q

Acetaminophen equal to NSAIDs in:

A

analgesia and antipyretic effects

355
Q

Acetaminophen is NO appreciable how

A

anti-inflammatory effects and anti-coag effects

356
Q

Acetaminophen is NO appreciable how

A

anti-inflammatory effects and anti-coag effects

357
Q

Acetaminophen is NO appreciable how

A

anti-inflammatory effects and anti-coag effects

358
Q

Acetaminophen is NO appreciable how

A

anti-inflammatory effects and anti-coag effects

359
Q

Acetaminophen high dose are

A

toxic to liver

360
Q

Acetaminophen high dose are toxic to liver

Acetaminophen >

A

N-acetyl-p-benzoquinoneimine (NAPQI) and quickly detoxified by glutathione to the product mercapteric acid which is sent to the kidneys for excretion

361
Q

Acetaminophen high dose are toxic to liver

Acetaminophen >

A

N-acetyl-p-benzoquinoneimine (NAPQI) and quickly detoxified by glutathione to the product mercapteric acid which is sent to the kidneys for excretion

362
Q

glutathione to the product mercapteric acid which is sent to the kidneys for excretion rxn occurs sufficiently at

A

moderate [ ], yet at high dosages, this rxn cannot keep up and NAPQI [ ] build up to toxic levels, inducing hepatic necrosis

363
Q

What if it is a normal dose, yet compromised liver?

A

Ask profess.

The liver will not process it rgith

364
Q

What if it is a normal dose, yet compromised liver?

A

Ask profess.

The liver will not process it rgith

365
Q

erythema

A

redness of the skin or mucous membranes, caused by hyperemia of superficial capillaries. It occurs with any skin injury, infection, or inflammation.

Medical Perspectives 411 (9 decks)

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