Shoulder Pathophysiology / 3 Flashcards
adaptively shortened connective tissue of shoulder joint
adhesive capsulitis
loss of integrity of motor unit in shoulder
rotator cuff tears
inflammation in any of the 4 rotator cuff tendons
rotator cuff tendinitis
most common location for rotator cuff tendinitis
supraspinatus
rotator cuff tendinitis is common with blank overuse
overhead
this is due to imbalances of the shoulder and can cause rotator cuff tendinitis
impingement syndrome
arthrokinematic glenohumeral instability that can lead to rotator cuff tendinitis is due to weakness of blank muscles
stabilizing
rotator cuff watershed area is where there is a blank and can lead to rotator cuff tendinitis
zone of weakness
zone of weakness of shoulder is where blank meets blank
subclavian, brachiocephalic
rotator cuff outlet reduction, active insufficiency of rotator cuff, abnormal scapulothroacic mechanics, passive capsule ligamentous insufficiency, and capsulo ligamentous laxity are all blank
impingement (external) etiology
impingement is caused by tissues thickening from blank
microtrauma
not all forward shoulders are caused by weak blank
trapezius
reduced supraspinatus outlet cause of impingement etiology is presents with a blank acromion, blank of C-A ligament, blank joint djd, enlarged blank tissues, or blank formation
abnormal, hypertrophy, ac, subacromial, spur
abnormal acromion that is flat
type 1
type 2 abnormal acromion is blank
smooth curve
abnormal acromion type 3 is blank
anterior hook
tight capsuloligamentous structure will contribute to a blank capsular constrain mechanism
hyper
in a passive capsulolig insufficiency, direction of the translation will be blank to the anatomic anatomical location of the blank strcuture
opposite, tight
passive capsuloligamentous insufficiency most commonly occurs during
overhead reaching
there is excessive blank humeral head translation during motion with a capsuloligamentous laxity
anterior
UNDER SURFACE OF posterior rotator cuff being impinged
internal shoulder impingement
posterior humeral head and glenoid are incriminated in blank impingement
internal
internal impingement when horizontal abduction is beyond the POS and scapular protraction/winging beyond normal POS
hyper angulation
internal impingement comes with an anterior blank laxity
capsuloligamentous
GH apprehension and relocation tests are for blank of internal impingement
capsuloligamentous laxity
glenohumeral is the most common area for blank tendinitis
calcific
calcific tendinitis is when calcium deposits into the substance of a blank
tendon
biceps tendon is cited to be the 2nd most common location of blank
shoulder tendinitis
bicep tendinitis is typical with athletes attempting to decelerate elbow blank and radioulnar blank during follow through
extension, pronation
overhead movements can cause blank biceps tendinitis
intraarticular
impingement, spur, subluxation can cause this type of biceps tendinitis
extraarticular
shoulder bursitis is not usually the blank cause
primary
shoulder bursitis is typically in the blank
subdeltoid
bursitis can become blank or develop adhesions
fibrotic
rotator cuff tears are the end of the blank process
degenerative (ct disease process)
full tears are classified by blank in rotator cuff
size
less than 1 cm rotatory cuff tear
small
less than 3 cm rotator cuff tear
medium
less than 5 cm rotator cuff tear
large
greater than 5 cm rotator cuff tear
massive
partial rotator cuff tears are classified by blank
location
two reasons rotator cuff tears don’t heal that well
tear bathed in synovial fluid, muscles retract from each other
most partial tears occur at blank age
around 40
three tests for rotator cuff tears
drop arm sign, painful arc (60-120), infraspinatus muscle test: resisted er in neutral
most full tears occur near blank age
about 70
blank percent recurrence rate of gh dislocation in younger patient
80-95%
most commonly dislocated joint and rate
gh, 1-2%
percent of traumatic gh dislocations
95%
percent of atraumatic gh dislocations
5 percent
most gh dislocations (98%)
subacromial
subacromial dislocation occurs blank to glenoid and blank to acromion
posterior, inferior
very rare gh dislocation that has extreme soft tissue damage
superior
gh instability may result from or contribute to gh blank or blank
subluxation, dislocation
gh blank is more difficult to diagnose than dislocation and how classified
subluxation, how far humeral head is out of glenoid
most common type of gh instability
anterior
glenohumeral capsule becomes inflamed, thickened, and fibrotic and adheres to itself or the humeral head
adhesive capsulitis
Matsen’s GH instability classifications TUBS and AMBRI
TUBS: Traumatic Unilateral Bankart Surgery
AMBRI: Atraumatic Multidirectional Bilateral Rehabilitation Inferior capsule shift
adhesive capsulitis is blank etiology
unknown
spontaneous atraumatic onset of adhesive capsulitis
primary classification
posst trauma, post immobilization, concurrent system disorder type of adhesive capsulitis
secondary classification
pain is during blank phase
freezing
stiffness is during blank phase
frozen phase
return to normal phase
thawing
frozen shoulders often last blank months per phase and blank to blank total
3-4, 6 months to 3 years
separation or subluxation of ac joint from moderate trauma can be a complete tear of ac ligament
ac joint injury grade 2
secondary to mild injury force and results in partial tearing of ac ligament fibers
ac joint injury grade 1
severe force, rupture ac lig and capsule and cc ligaments… aka ac joint dislocation
ac joint injury grade 3
clavicular fracture to middle third, most common
–MOI: “FOOSH” or lateral shoulder
group 1
clavicular fracture to lateral clavicle between coracoclavicular ligaments & AC joint
–MOI: downward force or fall on to the “point” of the shoulder. Often associated with AC separation
group 2
clavicular fracture to medial third, very rare seldom displaced
–MOI: direct blow from lateral shoulder
group 3
scapular fractures are very blank
rare
normal moi of scapular fracture
foosh
Common complication of “body’ fractures of scapula is blank of overlying muscles to scapula reducing mobility.
adherence
glenoid fossa fractures are associated with glenoid blank
dislocations
most common injury resulting from foosh
proximal humeral fractures
blank commonly fracture humeral heads and there is a blank ratio of women to men and often is caused by blank
elders, 2:1, osteoporosis
–Axillary nerve most common
–Brachial plexus: 6.1% frequency
–Avascular necrosis: 3-14% incidence in three part fractures
these are all blank complications associated with blank fractures
neural, humeral head
ra is a blank disease
systemic
Age for type I Neer’s impingement
Less than 25
Characteristics of type I Neer’s impingement (4)
- Edema
- Hemorrhage
- Inflammation
- Typically reversible
Treatment for type I Neer’s impingement (2)
- Avoid causitive ADLs
2. Improve biomechanics
Age for type II Neer’s impingement
25-40
Characteristics of type II Neer’s impingement (4)
- Bursa thickening
- Tendon fibrosis
- Pain recurrent
- Decreased chance of reversing
Treatment for type II Neer’s impingement (2)
- Add anti inflammatory
2. Consider surgery
For type II Neer’s impingement what is surgically removed (2)
- Subacromial decompression
2. Bursectomy
Age for type III Neer’s impingement
Older than 40
Characteristics of type III Neer’s impingement (3)
- HH and acromial bone spurs
- Tendon tears
- Progressive disability
Treatment for type III Neer’s impingement (2)
- Acromioplasty
2. RC repair
Is it more effect to go into hyperangulation when throwing or stop at the POS
Stop at POS
What are the classifications of partial RC tears (3)
- Articular side
- Mid substance
- Bursal side
What is the notch phenomenon
The progression of the RC tear
Example of notch phenomenon
Eventually supraspinatus tear will become large enough to include infraspinatus tear due to improper mechanics of the RC muscles
Age for type I Neer’s impingement
Less than 25
Characteristics of type I Neer’s impingement (4)
- Edema
- Hemorrhage
- Inflammation
- Typically reversible
Treatment for type I Neer’s impingement (2)
- Avoid causitive ADLs
2. Improve biomechanics
Age for type II Neer’s impingement
25-40
Characteristics of type II Neer’s impingement (4)
- Bursa thickening
- Tendon fibrosis
- Pain recurrent
- Decreased chance of reversing
Treatment for type II Neer’s impingement (2)
- Add anti inflammatory
2. Consider surgery
For type II Neer’s impingement what is surgically removed (2)
- Subacromial decompression
2. Bursectomy
Age for type III Neer’s impingement
Older than 40
Characteristics of type III Neer’s impingement (3)
- HH and acromial bone spurs
- Tendon tears
- Progressive disability
Treatment for type III Neer’s impingement (2)
- Acromioplasty
2. RC repair
Is it more effect to go into hyperangulation when throwing or stop at the POS
Stop at POS
What are the classifications of partial RC tears (3)
- Articular side
- Mid substance
- Bursal side
What is the notch phenomenon
The progression of the RC tear
Example of notch phenomenon
Eventually supraspinatus tear will become large enough to include infraspinatus tear due to improper mechanics of the RC muscles