KIN 428 Flashcards

1
Q

Definition of (neuro)musculoskeletal disorders?

A

Injuries and disorders of the muscles, nerves, tendons, and ligaments, joints, cartilage, bones, and spinal discs

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2
Q

MSD?

A

musculoskeletal disorder

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3
Q

WMSD?

A

Work-related musculoskeletal disorder

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4
Q

UEMSD

A

upper extremeity musculoskeletal disorder

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5
Q

CTD

A

cumulative trauma disorder

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6
Q

CTS

A

carpal tunnel syndrome

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7
Q

Estimated cost for overall MSD?

A

$254 billion in USA and $25 billion in Canada

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8
Q

Percentage of all claims to WSIB are from the upper extremity?

A

Approx. 30%, with the finger causing the most issues

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9
Q

Wide variation in estimates of specific UEMSD prevalence is due to?

A

Recording/reporting of injuries, definition of a disorder, and the population being studied

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10
Q

Prevalence vs. Incidence?

A

Prevalence is the portion of the population that already has the disorder/disease. Incidence is the portion of the population that newly has the disorder/disease.

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11
Q

What are the fastest growing cause of occupational disability?

A

UEMSD, especially the shoulder because they have the longest return to work (approx 45 days) because they are cumulative not traumatic injuries.

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12
Q

Students and MSD, who is protected and who is more at risk?

A

Protective: being a history major or an athlete. Risk: computer use greater than 20 hours per week, being a computer science major, and being female!

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13
Q

Percentage of GDP that is spent on MSds?

A

3.4-5%

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14
Q

Tissue types for UEDs?

A

tendon, ligament, muscle, nerve, vascular, bursa, cartilage, bone, other connective tissue (i.e. labrum)

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15
Q

Itis?

A

Inflammation

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16
Q

Syndrome?

A

Usually neural

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17
Q

Some examples of nerve disorders in the UE?

A

thoracic outlet syndrome, digital neuritis (bowler’s thumb),

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18
Q

Some exaples of tendon disorders in the UE?

A

Rotator cuff tendinitis, flexor tendinitis, ganglionic cyst

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19
Q

Some examples of muscle disorder in UE?

A

Focal dystonia, tension nexk syndrome

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20
Q

Some examples of vascular disorders in UE?

A

White finger, Raynaud’s syndrome

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21
Q

Role of the tendon?

A

Transmit forces from muscles to bones

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22
Q

Tenosynovitis?

A

Inflammation of the tendon and the tendon sheath. Really bad because the more that swells the more compression there is, increasing chances of nerve problems

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23
Q

Tendinitis?

A

Inflammation of JUST the tendon

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24
Q

Enthesopathy?

A

insertional tendonsitis…occurs at bond-tendon junction

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25
Q

Peritendinitis?

A

Central portion of the tendon, usually NOT the sheath

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26
Q

Myotendinitis?

A

Muscle-tendon interface inflammation

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27
Q

Examples of tendon disordrers?

A

Bicipital tendinitis (often common with rotator cuff injuries), lateral epicondylisis, trigger finger (debated if it is tendoninitis or tenosynovitis b/c there may be stenosis of tendon sheath)

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28
Q

3 mechanisms of tendon disorder development?

A
  1. Excessive and typically repetitive TENSILE loading 2. Compression 3. Tendon strength decreases with age
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29
Q

What does excessive and repetitive tensile loading do to a tendon?

A

Leads to an increase in capillaries (need more blood to enhance healing), inflammation (immune response), edema (bruising), microtears (stack enough of these = total tear), and fibre separation

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30
Q

What type of force on the tendon causes the most damage?

A

Transverse/compression because the collagen is not aligned in a way that it can handle forces perpendicular to it (like fibre optic cables)

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31
Q

Muscle function?

A

Initiate movement, generate force, stabilize joints, highly vascular and bring blood supply to the tendon. Actuators for the lever system of the skeleton.

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32
Q

Myalgia?

A

Muscle soreness and pain (local tenderness to touch)

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33
Q

Myositis?

A

Inflammation of muscle tissue

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34
Q

Myofascial pain syndrome?

A

Chronic myalgia, usually related to insufficient recovery (doing the same job over and over again)

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35
Q

Fibromyalgia/fibrositis?

A

End stage of myalgia…spastic muscles, tingle (nerve commponent), nervousness, sleeplessness.

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36
Q

Why does MSK pain increase at night?

A

Not distracted by the day’s activities anymore, so people concentrate on their pain.

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37
Q

Examples of muscle disorders?

A

Tension-neck syndrome (people at poor work stations, common in clerical professions, hunched shoulders). Writer’s cramp (focal dystonia, overgrip between 5-10x the required force). CTS and finger force are related.

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38
Q

Mechanisms of muscle disorder development?

A

External force on passive tissues…stretch in eccentric contractions. L-T relationship…stretching passive tissues then putting load on top of that, leads to sarcomere strain, but recovery is fast (slows with age)

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39
Q

Nerve function?

A

Send signals through the body (commands and feeback are used to assess after an injury)

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40
Q

What is nerve entrapment?

A

Nerve trapped between 2 tissues (muscle, bones, connective tissues)

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41
Q

What does nerve entrapment cause?

A

Impaired blood flow, which decreases oxygen to a tissue, leading to tissue death. Entrapment can also cause the mechanical blocking of depolarizations, which leads to atrophy

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42
Q

Double crush syndrome?

A

The existence of 1 entrapment increases the likelihood of another axonal flow disruption…nerves can be greater than 1 metre long, so lots of opportunities to get crushed along the way…CTS surgery when the problem is actually at the elbow

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43
Q

Digital neuritis?

A

Nerve inflammation due to direct pressure in fungers and thinb

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44
Q

Examples in UE nerve disorders and the nerve affected?

A

CTS (median verve), Cubital Tunnel Syndrome (ulnar), Pronator Teres Sydrome (median nerve), Thoracic Outlet Syndrome (Brachial Plexus), Bowlers Thumb (exmaple of digital neuritis…direct pressure of bowling bowl on ulnar nerve in the thumb0

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45
Q

Mechanisms of nerve disorder development?

A
  1. Compression of the nerve 2. Vibration accelerates the process through a series of microdamages to the nerve 3. Direct compression leads to intraneural edema (bruising) and fibrosis
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46
Q

What does compression to a nerve cause?

A

It causes damage, which leads to an inflammatory response, fibrin deposits are laid in an attempt to heal the nerve, leading to fibrous tissue, which leads to more compression, and eventually axonal degeneration.

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47
Q

Role of vasculature?

A

Provides materials to cells for normal functions…especially O2

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48
Q

Ischemia?

A

Decrease in blood flow to a body part caused by obstruction or constriction of blood vessels

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49
Q

When is ischemia of greatest concern?

A

During fractures…if the bone fragment dies, the doctors must digure out hoe to reconstruct bone without the dead piece (huge problem with the femoral and humeral head)

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50
Q

Examples of vascular disorders in the UE?

A
  1. Hand-Arm Vibration Syndrome (HAVS) 2. Raynaud’s Syndrome/White Finger 3. Hypothenar Hammer Syndrome (ulnar artery)
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51
Q

Precipitating factors for vascular disorders?

A
  1. Vibration 2. Cold temperatures 3. Direct Pressure
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52
Q

Definition of bursa?

A

Sack of sack-like body cavity that usually contains synovial fluid and is usually around joints (articulations) and “exposed” bones. Role is to reduce friction focal forces and distribute them

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53
Q

Bursitis?

A

Inflammation of the bursa

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54
Q

Causes of bursitis?

A
  1. Friction (cartilage degraded, then bone on bone happens, and so do bone chips) 2. Trauma 3. Inflammatory Disease (rheumatoid arthritis) 4. Bacterial infections
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55
Q

Bursitis locations in the UE?

A

Elbow (exposed bone) and shoulder (sub-acromial…inflamed bursa = impinges supraspiantus tendon)

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56
Q

Role of the bone?

A
  1. Form and protection 2. Factory for RBCs and Ca2+ storage 3. Attachment for muscles and form articulating joints for movement
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57
Q

Role of articular cartilage?

A
  1. Cushioning for joints 2. Support 3. Shock absoprtion/distribution (decreases stress risers)
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58
Q

Arthritis?

A

Joint inflammation…leads to pain, swelling, and stiffness (inability to move a joint)

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59
Q

Rheumatoid arthritis?

A

Subclass of arthritis that involves general/systemic imflammation throughout the body

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60
Q

Gout?

A

Specialized case of rheumatoid arthritis

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61
Q

Osteoarthritis?

A

most common arthritis…cartilage degeneration at a specific joint

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62
Q

Fractures?

A

Usually traumatic with the exception of stress fractures, which is due to the incomplete healing of microfractures

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63
Q

Age-related skeletal changes?

A
  1. Geometric (alter the mechanical properties, particularly load tolerance…causes more fractures) 2. Cortical (decrease in thickness and increase in porosity) 3. Trabecular (decrease in thickness and in number of trabeculau, making it easier to fracture the bone because of the loss of the ability to distribute and absorb force)
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64
Q

Why are older people very susceptible to crush fractures in the vertebrae?

A

Body keeps the bones it needs to support common forces and movements…most forces on the spine are vertical, so the most bone is left in a vertical fashion, making the vertebrae weakened to horizontal forces

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65
Q

What is the worst age range for bone loss in women?

A

50-80…menopause

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66
Q

Why do women age 50-60 present with more wrist fractures than hip fractures?

A

Women in this age group have longer strides and are moving faster than women 75+, so when they fall, they fall forwards, using their wrist to brace the fall. Women 75+ have smaller base of support due to small steps and slow gait, so when they fall, they fall backwards and fracture a hip.

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67
Q

What is the leading cause of disability over the age of 65?

A

Osteoarthritis

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68
Q

What is osteoarthritis?

A

Cartilage degeneration that is caused by the reduction in synthesis of cartilage matrix, which leads to bone on bone contact. This then decreases range of motion, which leads to compensations in movements. These compensations leads to bone spurs, which cause pain, and result in even more compensations, more bones spurs, etc…vicious cycle!!

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69
Q

What percentage of long-term disability in Canada is a result of arthritis?

A

25%…90% have dec. mobility, 66.6% have stair trouble, 62.7% cannot stand for extended periods of time, 51% have trouble picking things up from the floor, and 17.4% cannot dress themselves

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70
Q

Osteomalacia?

A

Demineralization of bones, which leads to deformities and fractures…usually linked to a vitamin D deficiency

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71
Q

Paget’s Disease?

A

Excessive bone resorption and overvascularized bones, which leads to brittle bones. This is a major cause of spinal compression fractures because trabecular bones is the first to be lost (soda can crushing analogy)

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72
Q

Age impact on connective tissue?

A
  1. General loss of elasticity with age, which comes along with increased stiffness, brittle tendons, and decreased regeneration capacity. This causes increased pathology of tendon tears because brittle tendons can tolerate even less transverse/compressive loads.
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73
Q

Physiological age related muscular changes?

A
  1. 20-40% decrease in muscular strength with age 2. Fibre de-inervation (leads to atrophy and increased MU recruitment for the same task, so increased fatigue) 3. Decrease the number of fibres 4. Fibre type composition changes (increase in percentage of Type I fibres, so more endurance, but cannot do things with intensity of speed) 5. Decrease in speed of contraction
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74
Q

When does the precipitous drop-off in muscle strength occur?

A

At about age 50…this is a problem because the average working age is 50, so people are expected to do the same type of work, but they now have decreased abilities…not good)

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75
Q

Anatomic age related muscular changes?

A

Loss of lean muscle tissue (i.e. muscle wasting)

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76
Q

Histochemical age related muscular changes?

A

Type II fibre atrophy, so % of Type I fibres increases. Loss of elasticity…decreases passive response, so must use more muscle to get things dones because force is from active and passive, but you now have less muscle fibres, so notgood…

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77
Q

Age related muscular pathologies?

A

Muscle cramping, myasthenia gravis, sarcopenia

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78
Q

What causes increased muscle cramping in older people?

A

Electrolyte imbalances caused by dehydration (neural drive for thirst decreases with age) AND spinal neuronal irritation

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79
Q

Myasthenia gravis?

A

Muscles become high fatiguable due to a defect in impulse transmission…antibodies block Ach receptors

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80
Q

Sarcopenia?

A

Gradual muscle loss tied to neural deficits

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81
Q

Age-related neural changes?

A
  1. Loss of neurons (mostly large neurons that are used for gross motor control, but also small neurons that control fine motor skills) 2. Action Potential Speed Reduction, which leads to a decrease in muscle contraction, and therefore force production. It is linked to vascular compromise (blood supply to nerve is lessened, leading to nerve death) 3. Homeostasis maintenance degrades (maintaining dopamine levels, causing motor tremors)
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82
Q

Age-related neural pathologies?

A
  1. Stroke 2. Dementia 3. Parkinson’s
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83
Q

What is a stroke, and how is it related to MSDs?

A

Acute ischemia to one section of the brain that causes a profound decrease in muscle function and motor control (AP not being sent down MN because brain is damaged?)

84
Q

What is dementia, and how does it relate to MSDs?

A

Alzheimer’s…visuospatial disturbance is common, which increases the risk of slipping and falling and not being able to catch themselves

85
Q

What is Parkinson’s and how does it related to MSDs?

A

It is a special dopamine problem that leads to motor tremors…this causes a need for increased tension in surrounding muscle to stabilize the tremor enough to do some tasks, this leads to MSDs

86
Q

Significance of Aging to UEDs?

A
  1. Prevalence increases as age increases 2. Systemic changes affect all joints 3. Treatment effectiveness modified by systemic diseases
87
Q

Why does the prevalence of MSDs increase with obesity?

A

Changes in motion patterns often cause MSDs…people with big guts commonly align themselves over the L4/L5 joint because this is the joint that is causing them problems, in return, they use their arms a lot for tasks, leading to a increase in UEDs

88
Q

How much is the OR increased for obese people and CTS?

A

2.5-3.4

89
Q

What is epidemiology?

A

Branch of medicine that studies epidemic diseases in a population

90
Q

Why is epidemiology relevant to MSDs (in and out of work)?

A

MSDs are reaching epidemic proportions due to the aging population and the increased awareness and reporting.

91
Q

Why do we have to learn about epidemiology?

A
  1. It is relevant to understanding research papers and dealing with incidence, prevalence, etc. of a particular disorder 2. Awareness of terminology…helps us to learn to “decode” articles and “decode” stats
92
Q

What are the 2 factors in an epidemiological study?

A
  1. Manipulation…control of exposure level and duration 2. Randomization…use of chance to assign exposures (this is sometimes hard to do, depending on what you are studying)
93
Q

General study types for epidemiology?

A
  1. Experimental/interventional…allows greatest control of subjects and exposure 2. Quasi-experimental…manipulate factors (not subjects) and there is NOT random subject population 3. Observational…weakest, but most common…look at exposure patters to draw inferences about disease etiology. Remember, though, observation is NOT causality
94
Q

If an odds/risk ratio is less than one, it is an…

A

benefit

95
Q

If an odds/risk ratio is greater than one, it is a…

A

hazard

96
Q

Odds ratios are used for what type of studies?

A

Observational/retrospective

97
Q

Risk ratios are used for what type of studies?

A

Experimental

98
Q

What is multi-variate modeling?

A

Looking at how multiple factors influence an outcome

99
Q

What do the letters in the multivariate modeling equation, y = Bo + B1x1 + … + E stand for?

A

Y is the output/outcome of interest. Bo is the bias/baseline. B are the coefficients. x is the factors/variables. E is the error term.

100
Q

In logistic multivariate modeling, what type of numbers of the factors?

A

Integers (like number of kids)

101
Q

In continuous multivariate modeling, what type of numbers are the factors?

A

Any value

102
Q

Temporality?

A

Exposure precedes the outcome

103
Q

Temporal contiguity?

A

Timeliness of the exposure…how long ago did the exposure occur

104
Q

COvariance?

A

Are things moving together…does decrease exposure decrease outcomes as well?

105
Q

Congruity?

A

Direct responses between exposures and outcomes…is there scalability? This is like a dose-response relationship…is 2x an exposure = to 4x injury?…very hard to establish with MSDs because there are multiple factors involved

106
Q

Plausibility?

A

Are things reasonably explainable by physiological, biomechanical, or neurological things? You should be able to identify some reasonable explanation of what you are observing.

106
Q

4 characteristics of the shoulder?

A
  1. Mobility 2. Instability 3. Geometric complexity 4. Experimental inaccessibility
107
Q

Joints that make up the shoulder joint?

A

Sternoclavicular, acromioclavicular, glenohumeral, and the sliding plane scapulothoracic

108
Q

Biomechanical property for motion?

A

Kinematics

109
Q

Biomechanical property for stability?

A

Constraints

110
Q

Biomechanical property for strength?

A

Force transmission

111
Q

Characteristics of the sternum?

A

The base of the arm
Attached to ribs by cartilage
Several palpable points (suprasternal notch And xiphoid)

112
Q

Characteristics of sternoclavicular joint?

A
  1. Relatively low intrinsic stability
  2. Full disk that distributes pressure
  3. Ligaments provide joint stabilization and limit clavicle ROM
113
Q

How many DOF does the SC joint have?

A

3 degrees

114
Q

What type of movements occur at SC joint?

A

Only rotational

115
Q

Movements at the SC joint?

A
  1. Elevation/depression, 30-35 deg
  2. Anterior/posterior, approx 35 deg
  3. Long axis, approx 45-50
116
Q

SC joint translations are limited inferiorly and superiorly by?

A

Inf. by Articular contact, always need this to resist gravity
Sup. by costoclavicular complex

117
Q

What makes up the shoulder girdle?

A

Clavicle and scapula

118
Q

Major responsibility of shoulder girdle?

A

Position the glenoid and for postural support of the glenoid so it maintains position

119
Q

What is kinematic redundancy at the SC joint?

A

Can’t move just the clavicle or just the scapula, they move together

120
Q

Shape of clavicle?

A

Integral/s shaped

121
Q

Primary purposes of clavicle?

A

Muscle attachment, allows some scapular positioning, and acts a strut to provide postural support

122
Q

What is the sole articulation between the scapula and clavicle?

A

Acromioclavicular joint

123
Q

Amount of rotation at AC joint?

A

Approx 20 degrees

124
Q

Where does the majority of joint stability come from at the AC joint?

A

Almost entirely from ligaments (acromioclavicular and coracoclavicular?

125
Q

Ligaments of coracoclavicular joint?

A

Conoid and trapezoid

126
Q

Ligaments at AC joint?

A

Acromioclavicular and coracoclavicular (conoid and trapezoid)

127
Q

Movement acromioclavicular ligament resists at AC joint?

A

Ant/post and inf/sup

128
Q

At high displacements what ligament dominates at the AC joint?

A

Conoid

129
Q

Primary role of scapula?

A

Provides attachment for 14+ muscles

130
Q

What is the glenoid?

A

Shallow fossa for humeral articulation, so its positioning is very important so the muscles can act property

131
Q

Point of coracoid process?

A

Offers even more muscle attachment sites and increases the moment arm of pec minor

132
Q

DOF of ST gliding plane?

A

5…2 translational and 3 rotational

133
Q

3 rotational movements at ST gliding plane?

A
  1. Tipping 2. Rotation3. Pro/retraction
134
Q

Translational movements at ST gliding plane happen along?

A

Ribcage/torso

135
Q

Amount of abduction at GH joint?

A

Approximately 150 degrees, then ST comes in

136
Q

Flexion at GH joint?

A

Approximately 180

137
Q

Amount of int/ext rotation at GH joint?

A

180 total, about 90 each way

138
Q

DOF of movement at GH joint?

A

6

139
Q

Movements at GH joint?

A

Spinning, rolling , and sliding

140
Q

Articular stability at GH joint is affected by?

A

Geometry of the individual…stress risers exist at contact points and mismatch of articulating surfaces = bad

141
Q

3 types of glenoids

A
  1. Flat, little contact point and easy to move humerus 2. Curved, lots f contact and resists humeral movement 3. Concave, pivots around contact points on the rim = inc force at these points = rim fracture
142
Q

Articular version at GH joint?

A

Stability from bony structure, resists downward gravity resistance, difficult because scapula moves

144
Q

Why isn’t ST gliding plane a joint?

A

Not two bones and no capsule

145
Q

What is the labrum, and what is its role in the shoulder?

A

A rim of fibrous tissues (NOT fibrocartilage) that acts as a non-bony extension of the joint to increase the glenoid depth and increase the contact area for the humeral head.

146
Q

What do the bursae do at the shoulder joint?

A

Act as a buffer between acromion and head of the humerus. Protect tendons from bone contact (acromion)

147
Q

What happens to the labrum during again, and what implications does this have at the shoulder?

A

Labrum gets smaller with age, which decreases total joint surface area, which increases stress concentrations and decreases stability

148
Q

What are the contributors to stability of the GH joint?

A
  1. Muscle activity 2. Ligaments 3. Joint suction 4. Adhesion 5. Bony constraints
149
Q

Stability is ______________ at the GH joint?

A

Anisotropic…dpends on the position of the joint

150
Q

What role does the humerus play at the GH joint?

A

Attachment site for functional GH movement

151
Q

Primary shoulder muscle functions?

A
  1. Position the glenoid for maximum stability 2. Articulate the upper arm (enabling hand finger placement) 3. Ensure GH stability 4. Provide humeral (and whole arm) stiffness
152
Q

Shoulder muscle groups?

A
  1. Scapulothoracic (for positioning the glenoid) 2. Glenohumeral/humeroscapular (for humeral articulation and GH stability) 3. Multiple joint (humeroclavicular, calvicular/thoracic, forearm attaching, humerothoracic)
153
Q

Actions of pec minor, a ST muscle?

A

Protraction, depression, medial rotation

154
Q

Action of rhomboids?

A

scapular retraction/elevation

155
Q

Actions of serratus anterior?

A

Scapular protraction, scapular lateral rotation

156
Q

Actions of levator scapulae?

A
  1. Lateral rotation 2. Elevation of superior angle
157
Q

Actions of trapezius?

A
  1. Scapular retraction 2. Elevation 3. Lateral Rotation
158
Q

Actions of middle deltoids?

A
  1. Scapular elevation 2. Abduction (coronal plane)
159
Q

Actions of anterior deltoids?

A
  1. Elevation (scapular place) 2. Flexion 3. Horizontal adduction
160
Q

Actions of posterior deltoids?

A
  1. Abduction (coronal plane) 2. Horizaontal abduction
161
Q

3 parts of the deltoid

A

middle, anterior, and posterior

162
Q

4 muscles of the rotator cuff?

A

supraspinatus, infraspinatus, subscapularis, and teres minor

163
Q

Action of supraspinatus?

A

Elevation

164
Q

Action of infraspinatus?

A

External rotation

165
Q

Actions of subscap?

A

Internal rotation

166
Q

AActions of teres minor?

A

External rotation

167
Q

Actions of teres major?

A

Internal rotation, adduction, extension

168
Q

Actions of coracobrachialis?

A

flexion and adduction

169
Q

Lat dorsi actions?

A

internal humeral roation and humeral adduction

170
Q

Pec major actions?

A

flexion, internal rotation, adduction, horizontal adduction

171
Q

Bicep action?

A

Elbow flextion, forearm supination, and humeral depression and stabilization

172
Q

Triceps action?

A

Elbow extension and scapular contributions

173
Q

Actions of sternocleidomastoid?

A

Neck movement

174
Q

Actions of sternohoid?

A

Hyoid position control

175
Q

Actions of subclavius?

A

Stabilize SC joint

176
Q

What innervates “the shoulder?”

A

Beachial plexus…many divisions and is the beginning of the UE peripheral nervous system

177
Q

Arteries that vascularize the shoudler?

A

Subclavian –> axiallry –> brachial

178
Q

Veins that vascularize the shoulder?

A

Axillary and cephalic

179
Q

What is the progression that leads to a change in tissue state?

A

Pathologies change movement –> change loading –> change tissue state

180
Q

What is laxity at the GH joint?

A

Asymptomatic…passive translation in GHJ, and is needed for movement

181
Q

What is instability at the GH joint?

A

Pathological…pain/discomfort/excessive translation (subluxation or dislocation)

182
Q

GH Stability in detail

A
  1. No deep stabilizing socket and minimal rim resistance = instability and flexibility 2. No isometric ligament contributions (variable ligament engagement depending on the activity)
183
Q

Basic laws of GH stability?

A
  1. The GHJ won’t dislocate as long as the net humeral joint reaction force (NHJRF) is directed within the effective glenoid arc. 2. The humeral head will remain centered in the glenoid fossa if the glenoid and humeral joint surfaces are congruent and the NHJRF is directed within the effective glenoid arc.
184
Q

What is the net humeral joint reaction force a resultant of?

A

Active muscle contraction, passive ligament stretch, intertial forces, gravitational forces, externally applied forces…Has a magnitude and a direction

185
Q

What is the effective glenoid arc?

A

The arc of the glenoid available to support the humeral head in a given configuration (direction)

186
Q

What is the effective glenoid arc a combination of?

A

Glenoid shape (bone) and labrum condition/deformation

187
Q

What is a glenoidogram?

A

Represents how the glenoid works. It is the path taken by the centre of the humeral head as it is translated away from the center of the glenoid fossa in a specific direction under defined loads. The shape indicates the extent of the effective glenoid arc in that direction.

188
Q

What is the balance stability angle?

A

The maximal angle that the NHJRF can make with the glenoid center line in a given direction

189
Q

In order for the GHJ to be stable, where must the NHJRF be directed?

A

Within the balance stability angles and the effective glenoid arc

190
Q

What is the stability ratio?

A

The maximal shear force in a given direction that can be stabilized by specific compressive loads assuming frictional effects to be minimal

191
Q

Static contributors to GH stability?

A

Articular version, articular conformity, labrum, ligaments, adhesion, suction cup

192
Q

Dynamic contributors to stability at the GHJ?

A

Active muscle force and proriorecption

193
Q

What is the glenoid version?

A

The angle that the glenoid centre line makes with the place of the scapula. The glenoid centre line usually points a few degrees posterior to the plane of the scapula.

194
Q

What does intra-articular pressure do?

A

Decreases translations in the joint. No pressure = too much laxity. Too much pressure = no translation/frozen shoulder

195
Q

How do ligaments contribute at the GHJ?

A
  1. Checkreins…keeps joint in position where muscles can contribute active stabilization 2. Coutnervailing forces…compression forces (push humeral head into glenoid), decreases displacement, and allows more shear
196
Q

What are the 2 results of muscle activity at the GHJ?

A

Rotation and contribution to joint forces (stabilizing and destabilizing)

197
Q

Passive contributors to GH stability?

A

Adhesion…wet surfaces are held together by molecular attractions. Suction cup…stability by pressure differentials between bones surfaces and intra-articular pressure around joint, highly dependent on joint uniformity

198
Q

What are mechanotransducers, and how do they relate to GH stability?

A

They transmit info about joint position and motion and encourage reflexive rotator cuff muscular action, which increases GH stability.

199
Q

What is decreased in unstable shoulder?

A

Decreased propriorecption

200
Q

How do glenoid rim fractures compromise GH stability?

A

Decrease stability tolerance in direction of defect

201
Q

What is the problem with improper repair of Bankart Lesions?

A

If it is a suboptimal versus an anatomic repair, the effective glenoid arc hasn’t really been recreated, so it’s just like not doing anything at all except there will be a tiny bit a labral check rein

202
Q

What causes muscle imblance/retroversion?

A

A misaligned joint reaction force due to a muscle not being able to generate fore OR an abnormal glenoid version that leads to the glenoid losing its shape and losing ability to resist shear

203
Q

What is Codeman’s Paradox?

A

You can get to the same spot in multiple ways, so it makes describing a movement at the GH joint very difficult

204
Q

What is shoulder rhythm?

A

Scapular and clavicular positions are dependent on relative position of humerus and torso…kinematic redundancy

205
Q

Is shoulder rhythm always right?

A

Rhythm is slightly different for each individual, so there are consequences when clinicians assess everyone thinking they all have the same rhythm

206
Q

How does posture affect muscles?

A

Postural moment arm changes due to placement of muscles and movement of bones