Week 4: Multifactorial/Multicomponent MSK conditions Flashcards

1
Q

What aggravates PFP

A

tasks that increase patellofemoral joint loading
such as
- jumping, running, squatting, stairs, prolonged sitting

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2
Q

Differentials for PFP

A
chrondomallacia patella 
patellar tendinopathy 
osgood schlatters
sinding larsen-johansson's disease 
bursitis 
pleural of neuromas 
intra-articular pathology
plica syndrome
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3
Q

What is the most common alternative diagnosis to PFP

A

patellar tendinopathy

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4
Q

How to differentiate between PFP and patellar tendinopathy

A

Onset
running, stairs, WB knee flexion vs jumping, change direction, stairs

pain
nonspecific, vague vs patella inferior pole

Aggrav
activities that load PFJ vs jumping, early to mid squat

Inspection
normal or VMO wasting vs general quads wasting

TOP
medial, lateral patella facets, inf patella or non vs inferior pole and possibly tibial tuberosity, rare mid tendon

Swelling
occasional vs tendon thickening

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5
Q

Differentiation #2

A

click, clunks and crepitus
give way = occasionally
knee ROM = normal, reduced in severe cases vs normal with OP

Quads concentric contraction = normally no pain but not quality vs possibly painful

PFJ= potential restriction any direction but commonly medial vs normal unless combined with PFPS

VMO =potential for weakness & deficits in tone and timing vs general quads weakness

function = stairs & squats may aggrav, PFJ taping decreases pain vs decline squat aggravtes, PFJ tape less effect

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6
Q

Extrinsic factors that lead to PFP

A

excess training load
altered training surface
incorrect footwear

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7
Q

intrinsic factors that lead to PFP

A
gender
weak medial
tight lateral
torsion of the femur /tibia 
eversion of the foot
 larger Q angle 
sulcus sign 
patella tilt 
decreased abduction strength of the hip and decreased ER strength of the hip lead to lower knee peak extension torque
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8
Q

Proximal treatments of PFP

A

hip abductor and ER strengthening

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9
Q

Distal treatment for PFP

A

orthoses

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10
Q

Local treatment for PFP

A

taping
PF mobes
vasti retraining

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11
Q

what is considered gold standard approach to treatment for PFP

A
multimodal approach 
including taping
vasti retraining
gluteal strength 
patella mobes and stretches
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12
Q

Sum up conservative treatment success for PFP

A

high success rate short term but long term is questionable

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13
Q

what is the role of supraspinatus

A

superior role of HOH
compresses HOH into glenoid fossa
restricts excessive superior translation of humerus

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14
Q

role of infraspinatus, teres minor and subscap

A

depression force on HOH

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15
Q

Role of infraspinatus and teres minor together

A

externally rotate humerus

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16
Q

Primary external impingement is

A

abnormalities of superior structures encroach into subacromial space
undersurface of the acromion may be beaked, curved, hooked
thickening of the coracoacromial arch or osteophytes on inf AC joint in older populations

17
Q

Secondary external impingement includes

A
excessive angulation (anterior tilt and IR) of acromion due to inadequate muscular stabilisation of scapula in younger athletes 
- altered activation patterns or strength imbalances (eg. deltoid vs RC)

RC tendons weakened by large volumes of activity

18
Q

Internal impingement is

A

occurs mainly in overhead sportspeople during late cocking stage of throwing (ext, abd+ER)
RC undersurface impinged against posterosuperior glenoid surface

may become pathologic due to repetitive trauma/overuse and injury to superior labrum

19
Q

Tendinopathy development involves

A

tendon becoming swollen and hypercellular
collagen matrix disorganised and tendon is weaker
increased vascularity and nerve density

volume is major determinant

20
Q

3 stages of tendon pathology

tendon pathology continuum

A

reactive tendinopathy

  • non-inflammatory proliferative response
  • acute overload

tendon dysrepair

  • similar, but greater matrix breakdown
  • chronic overload

degenerative
-progression of both matrix and cell changes/breakdown
areas of cell death
Ageing or chronic overload

21
Q

clinical presentation of supraspinatus tendinopathy

A

complaints of pain with overhead activities
activities <90 degrees may be pain free
ER can be a problem
possible Hx of associated symptoms of instability including recurrent subluxation
Episodes of dead arm
night pain is extremely common
difficulty sleeping
symptoms may be reproduced with impingement tests
EOR passive flexion - symptomatic
Resisted supraspinatus contraction
- resisted upward movement in 90 degrees abduction, 30 degrees horizontal flexion +IR
MRI = investigation of choice to determine presence of partial tears

22
Q

treatment of supraspinatus tendinopathy #1

A

avoid aggrav activities
Ice
single corticosteroid injection

23
Q

treatment of supraspinatus tendinopathy #2

A
correction of abnormalities 
GH instability 
Muscle weakness or imbalance 
ST tightness
Impaired scapulohumeral rhythm 
Training errors
24
Q

Exercise therapy for the shoulder

A

the shoulder is highly muscular dependant
muscle recruitment patterns, coactivation and force couples are vital for normal function
minimise pain to avoid pain inhibition
- pain relief is a key to success

25
Exercise rehab for supraspinatus tendinopathy can include
addressing decreased rotator cuff strength or imbalance - target ERs Restore correct SH rhythm Stretching of the posterior capsule + Tx spine mobilisation
26
Closed chain exercises can be used in supraspinatus rehabilitation, what are the suggested parameters
proximal to distal sequencing allows optimum force generation safe muscle loads and activation levels decreases tensile stresses on ligament and tendons enhances proprioceptive function provides stability to the ST joint force closure to the GH joint abnormalities along the kinetic chain must be identified and corrected - training errors such as technique and overuse should be corrected-
27
Plyometrics for supraspinatus rehabilitation
development of power utilise stretch-shortening cycle heightens excitability of nervous system goal is to decrease amortization time phase
28
What is a SLAP lesion
due to excessive traction through labrum via LH biceps extend from ant to biceps tendon to posterior to tendon stable or unstable depending on amount of superior labrum and LH biceps tendon firmly attached to glenoid margin 4 types - classification Non-Slap - degenerative, flap and vertical labral tears, Bankart lesions, Hill-Sachs
29
the 4 types of SLAP lesions are
Type 1: attachment of the labrum to glenoid attached but fraying and degeneration present Type 2: lesions with detachment of Sup labrum and LH biceps tendon from glenoid rim Type 3: meniscoid superior labrum torn away & displaced into joint but tendon & its labral rim attachment intact Type 4 : tear of sup labrum extends into tendon and these are displaced into joint
30
Clinical presentation of glenoid labrum injuries
Hx - often MOI or excessive traction on labrum via LH biceps Pain in posterior or posterosuperior joint line esp in abduction pain increased by overhead and HBB positions popping, catching, grinding TOP ant shoulder pain on resisted biceps contraction dynamic labral shear test +ve MRI often unnecessary with combination of clinical tests more sensitive
31
Treatment of glenoid labrum injuries
conservative Mx is generally unsuccessful except in extremely minor cases (always SLAP type 1) -if so, avoid heavy weights surgical repair generally indicated -arthroscopic SL repair +/- debridement Post surgery - exercise program - no gold standard Evidence on rate of return to participation post surgery is in consistent - return to pre injury levels of participation in athletes that perform overhead activities consistently lower than non-throwing/non overhead athletes