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

Tendon, ligament and muscle conditions Flashcards

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
Q

What are the clinical signs of the Tissue modelling phase

A

Stiffer/thicker tendon

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26
Q

Describe the pathology of the Tissue modelling phase

A

Fibrosis

Gradual change from collagen III to I

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27
Q

What are the treatment principles for the Tissue modelling phase

A
  • Increased loading and exercise programme
  • Improve fitness
  • Monitor progress by repeat ultrasound exam
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28
Q

What are the functions of skeletal, smooth and cardiac muscle?

A 
Skeletal = maintain posture, allow movement
Smooth = maintain position of fluids and move fluids
Cardiac = movement of blood
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29
Q

Disease of muscles are called?

A

Myopathies

30
Q

What are the features of myopathies in skeletal, smooth and cardiac muscle?

A 
Skeletal = weakness or spasm
Smooth = retention/incontinence, hypermotility or stasis
Cardiac = circulatory failure
31
Q

What my be found on the clinical exam in a patient with muscle conditions - acute and chronic?

A

Acute: swelling/pain
Chronic: stiffness, cramping, pain, fasciculations, weakness (differentiate from neurological conditions), atrophy, fibrosis/calcification

32
Q

Which 2 biochemistry tests can be used to diagnose muscle conditions?

A
  • Serum muscle enzymes (CK/AST/LDH)

- Urine sample

33
Q

How are serum muscle enzymes used to diagnose muscle conditions?

A
  • 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
Q

How is a urine sample used to diagnose muscle conditions?

A
  • 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
Q

Which muscle conditions can be detected using ultrasound?

A

Acute: haematoma
Chronic: fibrosis/calcification

36
Q

What is muscle atrophy?

A

Reduction in the size of muscles

37
Q

What are the causes of muscle atrophy?

A
  • Disuse: reversible if function restored
  • Denervation
  • Cachexia
38
Q

When is reinnervation of muscles possib;e?

A

If the nerve sheath is intact

39
Q

What are some causes of denervation in muscles?

A
  • 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
Q

When is net withdrawal of muscle protein (cachexia) seen?

A

Pregnancy

Rapid tumour formation

41
Q

What is hypertrophy?

A

Increased muscle bulk due to larger fibres and as a result of increased work load

42
Q

What happens to muscle fibres in hypertrophy?

A

Undergo longitudinal splitting

Sarcomeres, myofilaments and myofibrils added

43
Q

What are the three types of muscle degeneration?

A
  • Cellular swelling
  • Hyaline degeneration
  • Granular degeneration
  • increase in severity
44
Q

Describe cellular swelling

A
  • 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
Q

Describe hyaline degeneration

A
  • Affects the sarcoplasm but spares the sarcolemma

* Often seen with nutritional myopathies

46
Q

Describe granular degeneration

A
  • Severe damage with large basophilic granules of coagulated protein
  • Stain positive for calcium (mitochondrial overload)
  • Fibrosis or fat replacement
47
Q

How are calcification and ossification involved in repair?

A
  • Calcification due to irreversibly-damaged tissue

- Ossification where damaged tissue undergoes metaplasia to bone

48
Q

Each muscle fibres is served by how many capillaries?

A

3-12

49
Q

What are the consequences of blockage of the arterial supply to muscles?

A
  • 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
Q

What are the consequences of blockage of the venous supply from muscles?

A
  • 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
Q

How is Selenium/ Vitamin E used in the body?

A

As a part of the anti-oxidant system

52
Q

What are the consequences of Selenium/ Vitamin E deficiency?

A

If the anti-oxidant system is inefficient then there is damage to the cells within the body (particularly muscle cells) – white muscle disease

53
Q

Which animals are most commonly affected by Selenium/ Vitamin E deficiency?

A

Calves less than 6 months old

Beef calves from dams overwintered on poor rations

54
Q

What are the clinical signs of Selenium/ Vitamin E deficiency?

A
  • 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
Q

How is Selenium/ Vitamin E deficiency treated?

A

Parenteral administration of selenium/ Vitamin E

56
Q

Describe the features of stiff-lamb disease

A
  • 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
Q

How is stiff-lamb disease treated?

A

Parenteral administration of selenium/ Vitamin E

58
Q

Describe acute exercise-induced Exertional rhabdomyolysis (ER) in the horse

A
  • 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
Q

How is acute exercise-induced Exertional rhabdomyolysis (ER) in the horse diagnosed?

A

Clinical exam; muscle enzymes; myoglobinuria

60
Q

How is acute exercise-induced Exertional rhabdomyolysis (ER) in the horse treated?

A

Pain relief; fluid therapy; acepromazine (anxiolytic/vasodilation)

61
Q

Describe chronic exercise-induced Exertional rhabdomyolysis (ER) in the horse

A
  • 5% of TB racehorses; stress/nervous

- Poor performance/ stiffness/ ”cramps”

62
Q

How is chronic exercise-induced Exertional rhabdomyolysis (ER) in the horse diagnosed?

A

History; muscle enzymes; muscle biopsy (non-specific)

63
Q

How is chronic exercise-induced Exertional rhabdomyolysis (ER) in the horse treated?

A

Warm-up; avoid stress and high energy feeds

64
Q

Describe the features and clinical signs of eosinophilic myositis

A
  • 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
Q

Describe the features of eosinophilic myositis on histology

A

Central necrotic area with dead eosinophils and sarcoplasmic clumping; numerous eosinophils in periphery, some giant cells and inwardly radiating fibroblasts

66
Q

How is eosinophilic myositis treated?

A

Corticosteroids

67
Q

Name 2 bacterial conditions that affect muscles

A
  • Blackleg

- Malignant oedema

68
Q

Name 3 parasitic causes of muscle conditions

A
  • Trichonellosis (Trichenella spiralis in pigs)
  • Cysticercosis (Cysticercus ovis in sheep)
  • Toxoplasmal myositis
  • Sarcocysts (Sarcocytis tenella in sheep)
69
Q

Describe the features of toxic-atypical myoglobinuria

A
  • Atypical myoglobinuria in the horse
  • Horses at pasture
  • Unknown cause
  • Associated with sudden change in weather conditions
70
Q

What are the clinical signs of toxic-atypical myoglobinuria?

A
  • Acute onset, rapid and frequently fatal
  • Muscle weakness/recumbency
  • Increased CK/AST and myoglobinuria
71
Q

What will be seen in the PM of a horse with toxic-atypical myoglobinuria?

A

Widespread myonecrosis (skeletal and cardiac muscle)

Y3 MOD Orthopaedics (7 decks)

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