Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathology SEM 2 > MSK Pathologies > Flashcards

MSK Pathologies Flashcards

1
Q

Give the background Pathology of Lateral Epicondylitis ( Tennis Elbow)

A
  • Impacting the extensor muscles of the forearm
  • Age range 40/50s
  • Extensor Carpi Radialis Brevis most commonly affected
    • SUP , ECRL,ED,EDM,ECU
  • Caused by excessive/repetitive use
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How does pain present in Tennis Elbow?

A
  • Pain @ lateral epicondyle in line with extensors ( common extensor origin)
  • Varying in pain and severity
  • Aggs = Resisted wrist/finger extension/Supination
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How is Tennis Elbow managed?( not meds)

A
  • Load management
  • Exercise
  • Brace/taping
  • Eduction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How is Tennis Elbow managed? ( Medication)

A
  • NSAIDS
  • Corticosteroids
  • Shockwave Therapy
  • Surgery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Give the background pathology of Medial Epicondylitis ( Golfers elbow)

A
  • Pronator teres and Flexor Carpi Radialis
  • Pinching of the ulnar nerve
  • Females>Males
  • Less common
  • Aggs - Throwing and Gripping
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How is Golfers Elbow managed?( Not meds)

A
  • Load Mangement
  • Exercise
  • Brace and Trapping
  • Education
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Hows is Golfers Elbow managed?( Meds)

A
  • NSAIDS
  • Corticosteroids
  • Shockwave Therapy
  • Surgery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Give the background Pathology of De Quervains Tenosynovitis

A
  • Thickening of the tendon sheath around EPB and APL
  • May be spontaneous or initiated by overuse of the thumb( eccentric lowering of wrist into ulnar deviation)
  • Adhesions may develop
  • Pain on radial aspect
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How is De Quervains Tenosynovitis managed?

not meds

A
  • Finkelstein Test and Palpation
  • Load management
  • Exercise
  • Brace and Tapping
  • Education
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How is De Quervains managed medically?

A
  • NSAIDS
  • Corticosteroids
  • Shockwave therapy
  • Surgery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Using POLICE /PRICE give the management strategies for Strains/Sprains

A
  • Mobilising
  • Strength/Loading
  • Proprioception
  • Endurance training
  • Surgery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Give the background Pathology of Carpal Tunnel

A
  • Compression of the Medial nerve
  • 1/10
  • Common in females
  • Oedema , tendon inflammation , hormonal changes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How does Carpal Tunnel present?

A
  • Nocturnal Paraesthesia
  • Loss of sensation
  • Weakness of the muscles supplied by the median nerve
  • Pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How is Carpal Tunnel Managed?

A
  • Education
  • Load management
  • Splinting
  • Exercise
  • Corticosteroid injection
  • Surgery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is An Avulsion Injury?

A
  • Attachment site pulled away usually taking away a portion of the bone
  • For example- ASISw/Sartorius , AIISw/Rectus Femoris
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Give the background pathology of REDS and its meaning

A

REDS = Reduces Energy Deficiency Syndrome

  • Common in Teens/20s
  • Young Athletes
  • Resulting in Decreased body fat and can result in the loss of menstrual cycle in young women.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is Avascular Necrosis?

A
  • Loss of Blood Supply to the Bone

- Bone death=Bone Collapse.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What Causes Avascular Necrosis?

A
  • Trauma
  • Surgery
  • Steroid
  • Excessive Alcohol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is Hip Dysplasia?

A
  • Hip socket not covering full ball portion of the ball

head of femur

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Give the Background Pathology of Hip Dysplasia

A
  • Unstable , Shallow socket
  • Most common in females
  • Presents complications with age
  • Normal centre edge angle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Give the background pathology of a Labral Tear

A
  • Labrum
  • Common amongst athletes
    -End range position =Hyperextension , Hyperabduction and Hyper-flexion + External rotation
  • Injection to detect tear using MRI
    ( Gadolinium dye)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Give the background pathology of Greater Trochanteric pain Syndrome

A
  • Lateral Hip pain
  • Tendinopathy of Gluteus Medius and Minimus
  • Pressure of Illiotibial band
  • 40-60 yr old females
  • Post Menstrual
  • Lowering of Femoral Neck Angle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is Tendinopathy?

A

Active Process of Degeneration that involves Inflammatory Pathways

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Give the name tendons where tendinopathy occurs

A

-Achilles Tendon
-Patella Tendon
-Gluteal Tendon
-Hamstring Tendon
+ Upper Limb = Rotator Cuff , Long head Biceps , Lat and met Epicondylagia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Give the 3 stages of the Tendon Continuum

A

The reactive tendinopathy, tendon disrepair and the degenerative tendinopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Describe the changes to tendon cell population in Tendinopathy

A

Increased number of Tenocytes, Increased tenocytes metabolism , Increased immature Tenocytes, increased rate of apoptosis, immunoactive cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Describe the changes in collagen structure in tendinopathy

A
  • Reduction in Type I collagen
  • Organised areas with higher concentrations of immature collagen bundles (Type III)
  • linear fibres - unorganised smaller and irregular structure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Describe the Ground substance changes in Tendinopathy

A

PG and GAG ( Natural Lubricants) content alters , Increased H20 , Chemical Alterations , Substance P , Glutamate and Lactate.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Describe Neurovascularization in Tendinopathy

A

Influx of blood vessels into the anterior surface and mid substances , this is associated with various nerve fibres ingrowing into the Tendon.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Who gets tendinopathy?

A
  • Endurance runners
  • Older athletes
  • Active/athletic 40+
  • Changes in Loading
  • +60 yrs , adiposity, diabetes, inactive lifestyle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Give the background pathology of Adhesive Capsulitis ( Frozen Shoulder)

A
  • Excessive scar tissue or adhesions across GHJ - fibrosis
  • 3-5% general population
  • 20% obese/diabetes patients.
  • Resolution 1-3 years
  • Resulting in Stiffness, pain and Dysfunction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Give the two types of Adhesive Capsulitis ( Frozen Shoulder)

A

Primary - Spontaneous

Secondary-Trauma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

State the risk factors associated with Adhesive Capsulitis

A
  • Female>Male
  • > 40
  • Trauma
  • Diabetes
  • Hyperthyroidism
  • Cerebrovascular /Coronary artery disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Give the First Stage of Adhesive Capsulitis

A
  • Shoulder pain@night
  • Synovitis
  • Inflammatory cell infiltration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Give the second stage of Adhesive Capsulitis

A
  • Stiffness and pain
  • Synovitis
  • Loss of Axillary fold
  • Synovial Proliferation - dense fibrous tissue
36
Q

Give the Third stage of Adhesive Capsulitis

A

Global loss of ROM , with pain at End range

  • Synovitis resolved , however replaces by significant adhesions
  • Dense collagenous tissue
37
Q

Give the Fourth stage of Adhesive Capsulitis

A
  • Persistent stiffness w/minimal pain

- Advances adhesions

38
Q

Give the Management for Adhesive Capsulitis

A
  • Physiotherapy with early mobilisation and education
  • NSAIDS
  • Corticosteroid injections - Being careful of when in the disease process this is administered
  • Hydrodilation
  • Surgery (MUA , joint distension H20 and open surgical release)
39
Q

Give the Background Pathology of Osteoarthritis

A
  • Most common form of Arthritis
  • Can occur at any synovial joint
  • The pathogenesis of OA involves a degradation of cartilage and remodelling of bone due to an active response of chondrocytes in the articular cartilage and the inflammatory cells in the surrounding tissues.
40
Q

State the management strategies for osteoarthritis

A
  • Physio - mobilisations for pain and stiffness, ROM and strengthening exercises, lifestyle and weight loss
  • Corticosteroid injection
  • Surgery
41
Q

Give the Background pathology of Rheumatoid Arthritis

A
  • Systemic autoimmune disease
  • Synovium infiltration by immune cells
  • Osteoclast generation = bone erosion and loss of joint integrity
  • RA begins long before the onset of joint inflammation
42
Q

Give the risk factors associated with RA

A

-North America and Northern Europe
- Increase prevalence in females
-Increases with age
Pediatic = Juvenile idiopathic Arthritis.
-Smoking
-Air pollution
-Obesity
- Lack of Vit D

43
Q

Describe the Clinical presentation of Rheumatoid Arthritis

A
  • Polyarthritis of small joints of the hand
  • Joint stiffness in the morning
  • Fatigue
  • Deformity pain, weakness and restricted mobility in affected joints
  • If CX spine affected = cervical instability between C1 and C2
44
Q

State the management strategies of RA

A
  • Symptom management
  • Pharmacological management
  • nutrition
  • physiotherapy
45
Q

Give the background pathology of an Anterior shoulder dislocation

A
  • Arm positioned in abduction and external rotation
  • Humeral head displaces antero-inferiorly.
  • Can lead to Hill-sachs lesion/Bankart lesion
  • Concurrent rotator cuff injuries can also occur
  • Vascular and neuro structures at risk
  • Males
  • Younger patients
46
Q

Give the background pathology of an Posterior shoulder dislocation

A
  • 5% incidence rate
  • Blow to the front of the shoulder
  • Can also occur during seizures
  • Concurrent injuries to rotator cuff , ex-post labrum
  • Males
  • Younger patients
  • FOOSH
47
Q

Give the background pathology of Shoulder Instability

A
  • Disruption of dynamic/static stabiliser of the GHJ leading to dislocation, subluxation or apprehension
  • Traumatic or atraumatic
  • Ant, Post, inferior or Multidirectional
48
Q

State the clinical presentation of shoulder instability

A
  • Clicking /Pain
  • Sub-acromial signs
  • Rotator cuff signs
  • Positive apprehension test
  • Increased accessory movement at the GHJ
49
Q

Give the management strategies of Shoulder instability-

A
  • physiotherapy
  • Education
  • Motor control
  • Strength training
  • Proprioception training
  • surgery
50
Q

Give the Background Pathology of Dupuytrens Disease.

A
  • Nodular hypertrophy and contracture of the superficial palmar fascia ( Palmar aponeurosis)
  • Contracture of MCP and PIP = Loss of function
  • Slow occurrence
  • Thickening of the skin- Bands of fibrotic tissue - fingers impacted and pulling into flexion
  • Bilaterally
51
Q

State the risk factors associated with Dupuytrens Disease

A
  • Higher in males
  • Elderly
  • Strong genetic component
  • Alcohol ,smoking, manual labour
  • Associated with diabetes.
52
Q

State the management strategies for Dupuytrens Disease

A
  • Surgery
  • Fasciotomy - Least invasive - cut
  • Fasciectomy - removal
  • Dermofasciectomy - includes overlying skin ( Fat )
  • Amputation
  • Physiotherapy( post-op)
  • Splinting exercise
  • Education/advice
  • Oedema and Scar Management
53
Q

What are the two types of Meniscal Vascularisation?

A
  • Red-red region - Vascular

- White-white region - avascular , poor healing quality

54
Q

Give the types of Meniscal injury classification

A
  • Vertical longitudinal
  • Vertical horizontal
  • Horizontal
  • Oblique
  • Complex and degeneration
  • Bucket handle tear
55
Q

Give the background pathology of an ACL

A
  • More common
  • 15-25 sports
  • more common in women
  • Intra-articular
  • Knee is in flexion with valgus positioning , often causing trauma with rapid changes in direction.
  • Proximal = increased vascularity
56
Q

Give the Background pathology of an PCL

A
  • Less Common
  • Posterior force on proximal tibia.
  • Swelling , pain on kneeling , positive posterior drawer test
57
Q

What is Osgood Schlatter disease?

A

Irritation of occurring at the growth plate of the knee caused by too much tension on the patella tendon.
Common in young athletes

58
Q

Give the background pathology of patellofemoral joint pain

A
  • AKP
  • Tightening
  • Altered mechanics
59
Q

Give the symptoms of damage to lateral ligaments-

A
  • usually after traumatic event
  • pain =/tenderness
  • swelling/bruising
  • Muscle spasm
  • Inability bear weight
90
Q

Osgood- Schlatter Disease

A

Swelling and irritation of the growth plate tibial tubercle

Over use injury

91
Q

Sinding Larsen- Johansson Syndrome

A

Inferior pole of the patella - swelling and irritation of the growth plate

92
Q

Perthes Disease

A

Avascular necrosis of the femoral head - adolescence
Self limiting with revascularisation occurring within 2-4 years
2-12 years old , most common 6
Male:female , 4:1

  • reduce weight bearing
93
Q

Slipped Femoral epiphysis

A

Growth plate slipping at the hip.
Altering biomechanics
Can result in OA
Realignment with pins.

94
Q

Severs disease

A

Traction Apophysitis of the calcaneal insertion of the Achilles’ tendon

95
Q

Activity modification

A

Pain monitoring model 0-10
4-5 Caution - reduce exercise
6-10 stop - stop exercise allow to settle

96
Q

Why do weak muscles influence tendinopathy?

A

Good muscle contraction - increased energy efficiency, greater elastic recoil, less heat production , potential to improve and protection from tendinopathy

Poor muscle contraction / coordination - reduced energy efficiency, greater heat absorption , potential to trigger cellular response and tendinopathy, greater amplitude of tendon strain and accumulative load.

97
Q

Give 5 elements of a neuromuscular Achilles rehab program

A 
1 - ensure full dorsiflexion 
2- stop start movements at different positions 
3- make patient aware of any tremors 
4- add external load early in rehab 
5- different knee flexion angles
98
Q

Features of rehab post fracture

A 
1- restore function 
2- gait re-Ed 
3- ROM
4- strength training
5-Pain relief
99
Q

Management of Hamstring Strain

A
  • POLICE
  • early load
  • length of muscle ROM and stretch
  • strengthen
  • pain relief
100
Q

Posters-lateral complex injury

A

Rare but disabling
Poor outcome
Associated with PCL/ACL Injuries

Mechanism
Direct blow to anterior medial tibia in the extended knee
Fall into a flexed knee
Non contract hyper extension injuries

Some structures involved - ITB ,LCL, popliteus, ACL,lateral meniscus, biceps fem tendon etc

101
Q

Signs and symptoms of méniscal tears

A
  • catching
  • H/O loading and twisting
  • locking
  • effusion developing over 24hours
  • joint line tenderness
  • +ve clinical tests ( apley’s, mcmurrays)
102
Q

Overview of tissue rehab

A

Tendons - modify tissue , strengthen, progress , RTP
Joint/OA - Modify load , ROM, balance, strength, neuromuscular control MOI
Ligaments - Modify load, ROM, balance, strength , neuromuscular control MOI
Fractures and Joint replacements - ROM, strengthen, rehab function
Always remembering the wants and needs of the patient.
POLICE

103
Q

Give the diagnostic criteria of a frozen shoulder

A
  • Pain that comes on slowly and is felt at the deltoid region
  • Painful restriction of AROM and PROM in capsular pattern - LR-AB>MR + decreased ER
  • Inability to sleep on affected side
  • x-ray
104
Q

Signs and symptoms of rotator cuff tendinopathy-

A
  • Shoulder weakness
  • catching
  • full ROM - no limited end feel
  • Weakness and pain response on isometric resisted testing
105
Q

What is tendinitis?

A
  • Acute tendon overuse

- Often seen in young adults

106
Q

What is tendinosis?

A

Overloaded tendon condition with a degenerative, non-inflammatory pathology

107
Q

What is calcification?

A

Calcific deposits within tendon

108
Q

When referencing shoulder instability classification what is TAUBS

A

Primary classification - dislocation
T-raumatic
U-nidirectional - anterior most common 98%
B-ankhart lesion - Bankhurt reconstruction
S-urgery

  • positive apprehension test
109
Q

When referencing shoulder instability what is AMBRI?

A 
Secondary - Poor neuromuscular control 
A-traumatic 
M-ulti-directional
B-ilateral 
R-ehabilitation 
I-Inferior capsular shift

Positive Sulcus test

110
Q

What causes fall under the congenital classification of shoulder instability?

A
  • Osseous/labral defect

- Soft tissue abnormality

111
Q

S&S of Acromio-clavicular dislocation/subluxation

A

Common causes -
FOOSH
Contact sports
Fall onto point of shoulder

Signs and symptoms

  • Step deformity
  • Decreased HF/Elevation above 90 degrees
112
Q

State the management strategies of AC joint dislocation

A 
conservation-
-POLICE
-Mobilisation
-Active exs
Surgical 
-A/C joint stabilisation using coracohumeral ligament
113
Q

What management strategies would you recommend post fracture?

A

Soft tissue massage, particularly to manage Edema and swelling

Ice therapy

Stretching exercises to regain joint range of movement

Joint manual therapy and mobilisations to assist in regaining joint mobility

Structured and progressive strengthening regime

Balance and control work and gait (walking) re-education where appropriate

Taping to support the injured area/help with swelling management

Return to sport preparatory work and advice where required

114
Q

What are SLAP lesions?

A

SLAP lesion is mostly combined with a lesion of the proximal head of the biceps because it attaches on the superior part of the labrum glenoidalis. It is associated with pain and instability and an inability of the patient to perform overhead movements.

115
Q

What are Bankart lesions?

A

A Bankart lesion is a lesion of the anterior part of the glenoid labrum of the shoulder. This injury is caused by repeated anterior shoulder subluxations. The dislocation of the shoulder joint (anterior) can damage the connective tissue ring around the glenoid labrum.

116
Q

What is the background pathology of non-specific back pain?

A

Pathology SEM 2 (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions