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Y3 MOD Orthopaedics > Tendon, ligament and muscle conditions > Flashcards

Tendon, ligament and muscle conditions Flashcards

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1
Q

What are tendons and their functions?

A
  • Insertional points of muscles
  • Passively transfer force generated by muscle to bony attachments -> Leads to movement
  • Support joints
  • Store energy
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2
Q

What are ligaments and their functions?

A
  • Go from bone to bone
  • Attach/stabilise bones/joints e.g. cruciate ligaments, collateral ligaments
  • Protect tendons
  • Proprioception
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3
Q

What is the role of Tenocytes/ligamentocytes?

A

Responsible for the synthesis, maintenance and degradation of ECM

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4
Q

What are the 4 components of the ECM?

A

Collagen types, proteoglycans, elastin, water content

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5
Q

Which collagen types make up tendons and ligaments?

A
  • Tendon = 95% collagen type I and 1-5% type III

* Ligament = 90% type I and 10% type III

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6
Q

What is the role of collagen type III?

A

Acts to crosslink the main collagen fibres which run along the plane of force through a structure

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7
Q

What are the general considerations of tendon/ligament injuries?

A
  • Extrinsic - External trauma e.g. laceration
  • Intrinsic - Overload/ degenerative
  • Can initially appear as an acute injury but they have a chronic component
  • Location/type
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8
Q

What are the possible locations/types of tendon/ligament injuries?

A
  • Intrasynovial/extrasynovial i.e. inside or outside a tendon sheath
  • Origin/insertion/mid-body (myo-osseous)/ avulsion fracture
  • Extensor versus flexor tendon
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9
Q

What factors are involved in the diagnosis of tendon/ligament injuries?

A
  • History: age, type, previous injury
  • Recent exercise e.g. pulled up lame after a jump, or chasing a ball and twisted limb
  • Wound/laceration: remember end of tendon may not be at same level as wound due to recoil
  • Clinical examination: stance/gait
  • Palpation
  • Diagnostic imaging
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10
Q

What may be felt on palpation of a tendon/ligament injury?

A
  • Swelling, pain, oedema, effusion

- Range of motion/stability

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11
Q

Ability to extend the tarsus whilst the stifle is flexed in a horse is indicative of what injury?

A

Peroneus tertius rupture

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12
Q

Using ultrasound in tendon/ligament disorder can allow assessment of what features?

A
  • Change in cross sectional area
  • Inflammation: swelling/enlargement of the tissue which will present as a change in the cross sectional area (compare to the other side to see if one is enlarged)
  • Fibre echogenicity
  • Margination
  • Position
  • Focal lesion vs generalised changes
  • acute vs chronic
  • blood flow
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13
Q

What is Fibre echogenicity?

A

How dark/light the tissue is on the ultrasound machine

  • Anechoic/hypoechoic
  • Hyperechoic/mineralised
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14
Q

How does inflammation affect margination?

A

When its inflamed the margins become less clearly defined

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15
Q

Describe the pathophysiology of why intrinsic injuries occur

A
  • Loss of strain energy as heat (hysteresis)
    • 43-45C in core of tendon at gallop
    • Protein uncoupling -> damage
  • Although often acute onset, many intrinsic tendon/ligament injuries have an ageing/degenerative component
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16
Q

Describe the 3 repair phases of tendon/ligament injuries (they are slightly overlapping)

A
  • Acute inflammatory response which occurs as soon as the damage does
  • Within a couple of days (and lasting a few weeks) is the proliferative phase – migration of cells into the damaged area to start producing normal or repair tissue – want to manipulate this healing process so there isn’t too much scar tissue
  • Occurring over weeks/months/years is the tissue remodelling phase
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17
Q

Why is it important that an acute inflammatory response doesn’t last too long?

A

It can cause damage to the surrounding tissue

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18
Q

What is involved in the tissue remodelling phase?

A
  • Anti-fibrotic cytokines
  • ECM and collagen deposition
  • Collagen synthesis and degradation
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19
Q

What are the clinical signs of the acute inflammatory phase?

A

Lameness
Pain on palpation
Heat
Swelling

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20
Q

Describe the pathology of the acute inflammatory phase

A 
Haemorrhage
Inflammation
- Neutrophils
- Macrophages and monocytes
- Increased blood flow
- Oedema
- Proteolytic enzymes
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21
Q

What are the treatment principles for the acute inflammatory phase

A
  • Limit inflammation: Cold therapy/ NSAIDs/
    (corticosteroids)
  • Protect limb/reduce further damage/swelling
  • Supporting bandage (cast/splint)
  • Rest
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22
Q

What are the clinical signs of the reparative/proliferative phase

A
  • Reduction or absence of lameness
  • Resolution of signs of inflammation
  • Tendon still palpably enlarged and soft
  • Signs of re-injury if exercised too early
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23
Q

Describe the pathology of the reparative/proliferative phase

A

Angiogenesis
Fibroplasia:
++ fibroblasts, collagen III, small collagen fibrils formed

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24
Q

What are the treatment principles for the reparative/proliferative phase

A
  • Promote angiogenesis: tendon splitting, stem cells/platelet-rich plasma
  • Minimise formation of excessive scar tissue: stem cells/platelet-rich plasma, physio/ ultrasound therapy
  • Early exercise (if lesion filled in) -> positive effect on collagen type I
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25
What are the clinical signs of the Tissue modelling phase
Stiffer/thicker tendon
26
Describe the pathology of the Tissue modelling phase
Fibrosis | Gradual change from collagen III to I
27
What are the treatment principles for the Tissue modelling phase
- Increased loading and exercise programme - Improve fitness - Monitor progress by repeat ultrasound exam
28
What are the functions of skeletal, smooth and cardiac muscle?
``` Skeletal = maintain posture, allow movement Smooth = maintain position of fluids and move fluids Cardiac = movement of blood ```
29
Disease of muscles are called?
Myopathies
30
What are the features of myopathies in skeletal, smooth and cardiac muscle?
``` Skeletal = weakness or spasm Smooth = retention/incontinence, hypermotility or stasis Cardiac = circulatory failure ```
31
What my be found on the clinical exam in a patient with muscle conditions - acute and chronic?
Acute: swelling/pain Chronic: stiffness, cramping, pain, fasciculations, weakness (differentiate from neurological conditions), atrophy, fibrosis/calcification
32
Which 2 biochemistry tests can be used to diagnose muscle conditions?
- Serum muscle enzymes (CK/AST/LDH) | - Urine sample
33
How are serum muscle enzymes used to diagnose muscle conditions?
* CK = creatinine kinase * AST = Aspartate aminotransferase * If both of these were raised it would indicate muscle damage * CK spikes faster and is cleared faster than AST
34
How is a urine sample used to diagnose muscle conditions?
* Myoglobin = main muscle protein * Released into the bloodstream when there is damage. If it reaches a particular threshold it spills over into the urine and can be detected
35
Which muscle conditions can be detected using ultrasound?
Acute: haematoma Chronic: fibrosis/calcification
36
What is muscle atrophy?
Reduction in the size of muscles
37
What are the causes of muscle atrophy?
- Disuse: reversible if function restored - Denervation - Cachexia
38
When is reinnervation of muscles possib;e?
If the nerve sheath is intact
39
What are some causes of denervation in muscles?
- Trauma e.g. Laryngeal hemiplegia (damage to left recurrent laryngeal nerve), Canine brachial plexus in forelimb avulsion (e.g. RTA) - Myaesthenia gravis: defect at neuromuscular junction
40
When is net withdrawal of muscle protein (cachexia) seen?
Pregnancy | Rapid tumour formation
41
What is hypertrophy?
Increased muscle bulk due to larger fibres and as a result of increased work load
42
What happens to muscle fibres in hypertrophy?
Undergo longitudinal splitting | Sarcomeres, myofilaments and myofibrils added
43
What are the three types of muscle degeneration?
- Cellular swelling - Hyaline degeneration - Granular degeneration - increase in severity
44
Describe cellular swelling
* Minor chemical imbalances within the muscle e.g. Na+/K+ or ATP exhaustion leading to Ca2+ overload in mitochondria * Moderate swelling but nuclei remain normal
45
Describe hyaline degeneration
* Affects the sarcoplasm but spares the sarcolemma | * Often seen with nutritional myopathies
46
Describe granular degeneration
* Severe damage with large basophilic granules of coagulated protein * Stain positive for calcium (mitochondrial overload) * Fibrosis or fat replacement
47
How are calcification and ossification involved in repair?
- Calcification due to irreversibly-damaged tissue | - Ossification where damaged tissue undergoes metaplasia to bone
48
Each muscle fibres is served by how many capillaries?
3-12
49
What are the consequences of blockage of the arterial supply to muscles?
- Partial blockage of distal aorta/iliacs can cause an ischaemic paralysis e. g. aortic-iliac thrombosis in horses and saddle thrombi in cats with left sided cardiomyopathy
50
What are the consequences of blockage of the venous supply from muscles?
- Blockage of large veins leading to congestion with leakage of blood to muscles with eventual muscle necrosis and fibrosis - Feature of prolonged recumbency in large animals
51
How is Selenium/ Vitamin E used in the body?
As a part of the anti-oxidant system
52
What are the consequences of Selenium/ Vitamin E deficiency?
If the anti-oxidant system is inefficient then there is damage to the cells within the body (particularly muscle cells) – white muscle disease
53
Which animals are most commonly affected by Selenium/ Vitamin E deficiency?
Calves less than 6 months old | Beef calves from dams overwintered on poor rations
54
What are the clinical signs of Selenium/ Vitamin E deficiency?
* Muscle weakness/ stiffness, recumbency, dyspnoea (intercostals mm) * Arrhythmias/ murmurs when myocardium is affected * Myoglobinuria; Elevated CK, AST values * Serum/ whole blood levels of Selenium
55
How is Selenium/ Vitamin E deficiency treated?
Parenteral administration of selenium/ Vitamin E
56
Describe the features of stiff-lamb disease
* 2-4 week old lambs (up to 1yr) * Similar aetiology to white muscle disease (poor rations for ewe) * Neck and tongue muscles (young lambs) or shoulder, thigh, back and intercostal muscles (older lambs) * Similar appearance to calves but calcification often more pronounced
57
How is stiff-lamb disease treated?
Parenteral administration of selenium/ Vitamin E
58
Describe acute exercise-induced Exertional rhabdomyolysis (ER) in the horse
- Unfit horses; “tying-up”; “colic-signs” - Laminitis would be the 3rd differential for a painful, recumbent horse - Stiffness to severe pain/recumbency - Commonly gluteals, semitendinosus/ semimembranosus; biceps femoris (quadriceps, back)
59
How is acute exercise-induced Exertional rhabdomyolysis (ER) in the horse diagnosed?
Clinical exam; muscle enzymes; myoglobinuria
60
How is acute exercise-induced Exertional rhabdomyolysis (ER) in the horse treated?
Pain relief; fluid therapy; acepromazine (anxiolytic/vasodilation)
61
Describe chronic exercise-induced Exertional rhabdomyolysis (ER) in the horse
- 5% of TB racehorses; stress/nervous | - Poor performance/ stiffness/ ”cramps”
62
How is chronic exercise-induced Exertional rhabdomyolysis (ER) in the horse diagnosed?
History; muscle enzymes; muscle biopsy (non-specific)
63
How is chronic exercise-induced Exertional rhabdomyolysis (ER) in the horse treated?
Warm-up; avoid stress and high energy feeds
64
Describe the features and clinical signs of eosinophilic myositis
- Large breed dogs e.g. GSDs - Acute recurrent pain and mandibular immobility: immune mediated condition - Bilaterally enlarged temporal/masticatory muscles - High percentage of eosinophils in the blood
65
Describe the features of eosinophilic myositis on histology
Central necrotic area with dead eosinophils and sarcoplasmic clumping; numerous eosinophils in periphery, some giant cells and inwardly radiating fibroblasts
66
How is eosinophilic myositis treated?
Corticosteroids
67
Name 2 bacterial conditions that affect muscles
- Blackleg | - Malignant oedema
68
Name 3 parasitic causes of muscle conditions
- Trichonellosis (Trichenella spiralis in pigs) - Cysticercosis (Cysticercus ovis in sheep) - Toxoplasmal myositis - Sarcocysts (Sarcocytis tenella in sheep)
69
Describe the features of toxic-atypical myoglobinuria
- Atypical myoglobinuria in the horse - Horses at pasture - Unknown cause - Associated with sudden change in weather conditions
70
What are the clinical signs of toxic-atypical myoglobinuria?
- Acute onset, rapid and frequently fatal - Muscle weakness/recumbency - Increased CK/AST and myoglobinuria
71
What will be seen in the PM of a horse with toxic-atypical myoglobinuria?
Widespread myonecrosis (skeletal and cardiac muscle)

Y3 MOD Orthopaedics (7 decks)

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