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MODULE 7 - Skin and Bones > PATHOLOGY - Bone, Cartilage, Muscles and Tendons > Flashcards

PATHOLOGY - Bone, Cartilage, Muscles and Tendons Flashcards

1
Q

List five possible reactions bone can have following injury

A

Bone remodelling
Altered bone density
Endochondral ossification disruption
Rapid deposition of woven bone
Conversion of periosteum to bone

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2
Q

What is osteitis?

A

Osteitis is inflammation of the bone

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3
Q

What is periostitis?

A

Periostitis is inflammation of the periosteum

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4
Q

What is osteomyelitis?

A

Osteomyelitis is inflammation of the bone medullary cavity

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5
Q

What are sequestrum?

A

Sequestrum is a fragment of necrotic bone isolated from the blood supply and surrounded by exudate

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6
Q

What is the most common infectious agent that affects bone?

A

Bacteria

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7
Q

What are the two methods used by infectious agents to enter the bone?

A

Haematogenous
Direct entry

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8
Q

Why is the metaphyseal region of epiphyseal growth plates predisposed to haematogenous infection?

A

Branches of the metaphyseal artery form capillary loops at the metaphyseal side of epiphyseal growth plates which provides a large supply of slow flowing blood which encourages the deposition of infectious agents and the establishment of infection

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9
Q

What are the two main causes of a fracture?

A

Trauma
Pathology

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10
Q

What classifies as a pathological fracture?

A

A pathological fracture results from the break of a diseased or weak bone

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11
Q

What is a closed fracture?

A

Fracture where the skin is unbroken

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12
Q

What is an open fracture?

A

Fracture where the skin is broken

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13
Q

What is a simple fracture?

A

Clean break of the bone into two pieces

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14
Q

What is a comminuted fracture?

A

Fracture where the bone is shattered into fragments

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15
Q

What is a greenstick fracture?

A

Cortex is broken on one side of the bone but bent on the other side

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16
Q

What is a spiral fracture?

A

A spiral fracture is where the fracture line spirals around the bone due to a twisting or rotational force

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17
Q

What is an infraction?

A

Fracture of the trabeculae without the involvement of the cortex

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18
Q

What are the consequences of a type I or type II growth plate fracture?

A

Type I or type II growth plate fractures have few to no complications

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19
Q

What are the consequences of a type III, type IV or type V growth plate fracture?

A

Type III, type IV or type V growth plate fractures may lead to growth abnormalities as they directly involve the growth plate

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20
Q

What are the four critical factors of fracture healing?

A

Correct alignment
Lack of movement
Asepsis
Adequate blood supply

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21
Q

How should a stable fracture heal?

A

A stable fracture has been clinically immobilised at either end and will undergo callus formation

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22
Q

How should an unstable fracture heal?

A

An unstable fracture will undergo callus formation

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23
Q

How should a rigid fracture heal?

A

A rigid fracture requires surgical intervention to bring the two ends together and ideally results in healing by surgical fixation

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24
Q

What are the functions of the callus formed during fracture healing?

A

The callus encircles the fracture site where it bridges the gap between the bone and stabilises the area

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25
Q

What forms in the centre of the callus if the blood supply to the fracture site is inadequate?

A

Hyaline cartilage

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26
Q

What are the five steps of callus formation?

A

Haematoma formation
Inflammation
Primary callus formation
Secondary callus formation
Remodelling

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27
Q

Describe briefly the steps of callus formation

A
  1. Blood vessels and the periosteum are damaged causing the formation of a haematoma at the fracture site. This haematoma will clot which act as a provisional wound matrix
  2. Chemotactic agents trigger the recruitment of neutrophils to the injury site. Neutrophils carry out phagocytosis to remove any pathogens and debris
  3. Fibrous tissue and cartilage are deposited to form a primary callus which bridges the gap between the fracture site
  4. Osteoblasts produce woven bone which provides temporary stability and support
  5. Woven bone is gradually replaced by lamellar bone through the activity of osteoclasts and osteoblasts
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28
Q

What are the three main advantages to healing via callus formation?

A

Natural process
Minimal intervention required
Low cost option

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29
Q

What are the three main disadvantages to healing via callus formation?

A

Callus may not be able to stabilise the fracture
Callus formation takes time
A large callus may interfere with joint or tendon function

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30
Q

What is healing by surgical fixation?

A

Healing by surgical fixation brings the ends of the bone closer together which allows for direct osteonal bridging of the fracture site with no callus formation

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31
Q

If a fracture site has a gap less than 1mm in width, which type of bone do osteoblasts deposit?

A

Lamellar bone

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32
Q

If a fracture site has a gap more than 1mm in width, which type of bone do osteoblasts deposit?

A

Woven bone

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33
Q

What is the consequence of anoxia during fracture healing?

A

Anoxia during fracture healing leads to necrosis

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34
Q

What is the consequence of instability to the fracture site during fracture healing?

A

Instability to the fracture site can lead to pseudoarthrosis (bones do not correctly fuse)

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35
Q

Why should you never use metallic implants that are too large to stabilise a fracture?

A

Metallic implants that are too large can lead to a lack of mechanical force inflicted onto the bone which could lead to bone atrophy (due to disuse)

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36
Q

What is osteopetrosis?

A

Osteopetrosis is the deposition of excess bone due to a genetic or infectious defect in bone resorption

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37
Q

What is osteogenesis imperfecta?

A

Osteogenesis imperfecta is the deposition of too little bone due to a genetic mutation in the type 1 collagen gene

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38
Q

What is chondrodysplasia?

A

Chondrodysplasia is disproportionate dwarfism caused by a genetic mutation in the cartilage producing genes. This has a resulting effect on endochondral ossification

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39
Q

List three specific examples of chondrodysplasia

A

Lethal bulldog type bovine chondrodysplasia
Spider lamb syndrome
Texel sheep chondrodysplasia

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40
Q

What causes lethal bulldog type bovine chondrodysplasia?

A

Mutation in the gene encoding for aggregan proteoglycans

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41
Q

What causes spider lamb syndrome?

A

Mutation is the gene encoding for fibroblast growth factor receptor 3 (FGFR3) resulting in disorganised centres of ossification leading to abnormally sized, shaped and orientated bones

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42
Q

What causes texel sheep chondrodysplasia?

A

Autosomal recessive mutation of the SLC13A1 gene encoding for the sodium-sulphate co-transporter resulting in chondrolysis within the articular epiphyseal cartilage complex leaving clefts within the cartilage

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43
Q

What is osteochondrosis?

A

Osteochondrosis is the failure of endochondral ossification affecting the articular epiphyseal cartilage complex and the physeal growth plates

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44
Q

What are the three forms/stages of osteochondrosis?

A

Osteochondrosis latens
Osteochondrosis manifesta
Osteochondrosis dissecans

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45
Q

What is osteochondrosis latens?

A

Osteochondrosis latens is the focal ischaemic necrosis of the epiphyseal growth plates

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46
Q

What is osteochondrosis manifesta?

A

Osteochondrosis manifesa is the failure of the necrotic epiphyseal cartilage to ossify during endochondral ossification, resulting in the retention of this necrotic cartilage within the subchondral bone

i.e. becomes a focal failure of endochondral ossification

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47
Q

What is osteochondrosis dessicans?

A

Osteochondrosis dessicans extension of the focal necrosis into the articular cartilage, resulting in dissecting necrosis, cleft formation and articular cartilage flaps

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48
Q

How does physeal osteochondrosis differ from articular-epiphyseal complex osteochondrosis?

A

Physeal osteochondrosis is the retainment of hypertrophic chondrocytes resulting in a failure of endochondral ossification

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49
Q

Describe the pathogenesis of physeal osteochondrosis

A

An infraction can interfere with the vascular invasion required for endochondral ossification, leading to the persistence of the hypertrophic chondrocyte zone of the physeal growth plate and thus lead to cartilage retainment

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50
Q

What is cervical stenotic myelopathy (wobblers disease)?

A

Cervical stenotic myelopathy is osteochondrosis dissecans of the articular facet joints between the vertebrae resulting in intervertebral joint instability

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51
Q

What is osteoporosis?

A

Osteoporosis is a reduction in bone mass

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52
Q

What are three of the main causes of osteoporosis?

A

Malnutrition
Low dietary calcium
Androgen deficiency

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53
Q

What is osteomalacia/rickets?

A

Osteomalacia/rickets is a defect in the mineralisation of bone leading to soft bone formation

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54
Q

What is the main causes of osteomalacia/rickets?

A

Vitamin D deficiency

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55
Q

What is fibrous osteodystrophy?

A

Fibrous osteodystrophy is the replacement of bone by fibro-osseus tissue

56
Q

What is fibrous osteodystrophy commonly associated with?

A

Hyperparathyroidism

57
Q

List the six most common primary neoplasms of bone?

A

Fibroma
Fibrosarcoma
Chondroma
Chondrosarcoma
Osteoma
Osteosarcoma

58
Q

What is the main method of metastasis seen in an osteosarcoma?

A

Haematogenous metastasis

59
Q

What is an osteochondroma?

A

An osteochondroma is a cartilage-capped osseous outgrowth seen in young animals

Osteochondroma of the vertebral column
60
Q

Why does feline osteochondromatosis have a poor prognosis compared to other osteochondromas?

A

Osteochondromas should enlarge in synchrony with physeal growth and thus stop growing when the growth plates have closed, however, feline osteochondromatosis shows progressive growth even after skeletal maturity has been reached

61
Q

What is primary synovial chondromatosis?

A

Idiopathic nodular cartilaginous metaplasia of the synovium

62
Q

What is commonly associated with secondary synovial chondromatosis?

A

Degenerative joint disease (DJD)

63
Q

When articular cartilage lesions begin to heal, the lesion is often filled with fibrocartilage. What is the disadvantage of this?

A

Fibrocartilage does not have aggrecan proteoglycans and thus is not as resistant to mechanical forces compared to hyaline cartilage

64
Q

What is feline physeal dysplasia?

A

Feline physeal dysplasia is the persistence of dysplastic growth plates

65
Q

(T/F) Feline physeal dysplasia is more common in female, overweight cats

A

FALSE. Feline physeal dysplasia is more common in male, overweight cats

66
Q

Why is feline physeal dysplasia only clinically significant in the proximal femoral epiphyseal growth plate?

A

Feline physeal dysplasia causes growth plate fractures in the proximal femoral epiphyseal growth plate due to the mechanical force inflicted on this site

67
Q

What is degenerative joint disease (DJD)?

A

Degenerative joint disease (DJD), also known as osteoarthritis, is a multifactorial disease where articular cartilage breaks down over time

68
Q

What are the two predisposing factors to degenerative joint disease (DJD)?

A

Abnormal stresses on joints
Abnormal cartilage

69
Q

Describe the pathogenesis of degenerative joint disease (DJD)

A

A disruption in the balance between cartilage repair and degradation in favour of articular cartilage breakdown mediated by degenerative enzymes (such as MMPs and aggrecanases). This leads to the progressive loss of proteoglycans in the cartilage extacellular matrix (ECM) leading to fibrillation. Articular cartilage will eventually be completely eroded leading to the thickening of the subchondral bone known as eburnation

70
Q

List two examples of degradative enzymes which cause an imbalance between cartilage repair and degradation in degenerative joint disease (DJD)?

A

Matrix metalloproteinases (MMPs)
Aggrecanases

71
Q

What is fibrillation?

A

Fibrillation is the roughening of articular cartilage caused by the separation and loss of proteoglycans causing exposure of collagen

72
Q

What is eburnation?

A

Eburnation is the thickening of subchondral bone in response to the complete erosion of articular cartilage

73
Q

What are osteophytes?

A

Osteophytes are bony projections that form to attempt to stabilise a joint with degenerative joint disease (DJD)

74
Q

How does degenerative joint disease (DJD) effect the joint capsule?

A

Degenerative joint disease (DJD) causes fibrosis of the joint capsule

75
Q

How does degenerative joint disease (DJD) effect the synovium?

A

Degenerative joint disease (DJD) causes hypertrophy/hyperplasia of the synovial villi

Hypertrophied synovial villi
76
Q

What stimulates inflammation secondary to degenerative joint disease (DJD)?

A

In degenerative joint disease (DJD), the release of fragmented collagen and proteoglycans from the articular cartilage stimulated synoviocytes to secrete inflammatory mediators IL-1 and TNF-α

77
Q

What are the effects of IL-1 and TNF-α in degenerative joint disease (DJD)?

A

IL-1 and TNF-α increase matrix metalloproteinases synthesis and IL-1 stimulates fibroblasts to deposit excess collagen causing fibrosis of the joint capsule

78
Q

What are the three typical clinical signs of degenerative joint disease (DJD)?

A

Joint enlargement
Pain
Reduced joint range of movement

79
Q

What are two of the main classifications of degenerative joint disease (DJD)?

A

Infectious arthritis
Immune-mediated polyarthritis

80
Q

What are the three routes of entry used by pathogens to cause infective arthritis?

A

Direct entry
Secondary to bacteraemia
Spread from adjacent sites

81
Q

Name a zoonotic bacteria which causes infectious arthritis in pigs

A

Erispelothrix rhusiopathiae

82
Q

Which bacteria is a common cause of neonatal infectious arthritis on farms?

A

E. coli

83
Q

What are the two classifications of immune-mediated polyarthritis?

A

Erosive immune-mediated polyarthritis
Non-erosive immune-mediated polyarthritis

84
Q

What causes rigor mortis?

A

Rigor mortis is caused by an absence of ATP production

85
Q

What resolves rigor mortis?

A

Rigor mortis resolves during autolysis of the muscle

86
Q

What can be indicated by pale pink/white muscle upon gross examination?

A

Anaemia
Young animal
Ischaemic necrosis
Mineralisation

87
Q

What can be indicated by pale red muscle upon gross examination?

A

Congestion
Haemorrhage
Haemorrhagic necrosis
Inflammation

88
Q

What can be indicated by green muscle upon gross examination?

A

Eosinophilia
Severe putrefaction

89
Q

What can be indicated by tan-brown muscle upon gross examination?

A

Lipofuscin deposition

90
Q

What can be indicated by black muscle upon gross examination?

A

Melanosis

91
Q

What can be indicated by soft muscle upon gross examination?

A

Necrosis
Adipose tissue

92
Q

What can be indicated by firm muscle upon gross examination?

A

Fibrosis

93
Q

What can be indicated by hard muscle upon gross examination?

A

Mineralisation

94
Q

What are the five responses muscle can have to injury?

A

Hypertrophy
Apoptosis
Necrosis
Regeneration
Chronic myopathic change

95
Q

(T/F) Muscle atrophy is irreversible

A

FALSE. Muscle atrophy is often reversible

96
Q

What is segmental muscle degeneration/necrosis?

A

Partial degeneration/necrosis of the myofibril

97
Q

What is global muscle degeneration/necrosis?

A

Degeneration/necrosis of the entire myofibril

98
Q

What does muscle depend on the achieve successful regeneration?

A

Muscle depends on intact satellite cells and the basal lamina to achieve successful regeneration

99
Q

Describe briefly the process of muscle regeneration if both the satellite cells and the basal lamina are intact?

A
  1. Macrophages enter and phagocytose any pathogens or debris
  2. Satellite cells differentiate into myoblasts
  3. Myoblasts fuse to form myotubules
  4. Nuclei move to the periphery
100
Q

What is formed during muscle regeneration if the basal lamina is destroyed but the satellite cells are still intact?

A

Multinucleated giant cells

101
Q

List four possible aetiologies of muscle ischaemia

A

Blood vessel occlusion
External pressure on the muscle
Internal pressure on the muscle
Vasculitis

102
Q

What is myositis?

A

Inflammation of the muscle

103
Q

What are the three methods used by infectious agents to enter the muscle?

A

Direct entry
Haematogenous
Spread from adjacent sites

104
Q

Which species of bacteria release toxins which cause myonecrosis?

A

Clostridia

105
Q

Which protozoa commonly causes myositis in cattle?

A

Neospora caninum

106
Q

Which nematode commonly causes myositis in pigs?

A

Trichinella spiralis

107
Q

(T/F) Trichinella sprialis is a zoonotic parasite

A

TRUE.

108
Q

Which four muscles does Trichinella spiralis commonly encyst upon?

A

Tongue
Masticatory muscles
Respiratory muscles
Ocular muscles

109
Q

What are the three clinical signs of a heavy Trichinella spiralis infestation?

A

Weakness
Paralysis
Reduced responsiveness

110
Q

List three cestode larvae which cause myositis?

A

Cysticercus bovis
Cysticercus cellulosae
Cysticercus ovis

111
Q

Give an example of an immune-mediated disease which causes myositis

A

Masticatory muscle myositis

112
Q

Which breed of dog is predisposed to masticatory muscle myositis?

A

German Shepherd

113
Q

Which muscle is most likely to rupture due to trauma?

A

Diaphragm

114
Q

What causes X-linked muscular dystrophy?

A

X-linked muscular dystrophy is caused by an absence of the dystrophin protein

115
Q

What is the normal function of the dystrophin protein?

A

Dystrophin usually prevents muscle contraction induced damage

116
Q

How does X-linked muscular dystrophy present upon gross examination?

A

X-linked muscular dystrophy presents as multifocal, polyphasic
necrosis and regeneration of skeletal and cardiac muscle

117
Q

What causes white muscle disease?

A

White muscle disease is caused by a selenium deficiency

118
Q

How does white muscle present upon gross examination?

A

White muscle disease presents as multifocal, polyphasic necrosis and mineralisation

119
Q

List two examples of agents that cause muscular toxicity

A

Monensin
Coffeeweed

120
Q

How do toxic insults to the muscle present upon gross examination?

A

Toxic insults present as multifocal, mono/polyphasic lesions

121
Q

What causes exertional ‘capture’ myopathy?

A

Exertional ‘capture’ myopathy is causes by extreme exertion and restraint

122
Q

How does exertional ‘capture’ myopathy present upon gross examination?

A

Exertional ‘capture’ myopathy presents as multifocal, monophasic necrosis

123
Q

What are the two primary neoplasms of muscle?

A

Rhabdomyoma
Rhabdomyosacrcoma

124
Q

List two secondary neoplasms of muscle

A

Injection site sarcoma

Infiltrative lipoma

125
Q

Describe the structure of tendons

A

Tendons are made up of collagen bundles arranged around a central elongated tenocytes and capillaries

126
Q

What is the function of tenocytes?

A

Tenocytes repair the extracellular matrix when the tendon is injured

127
Q

What are the three phases of tendon healing?

A

Inflammation
Proliferation
Maturation

128
Q

What occurs during the proliferation phase of tendon healing? (3 - 6 weeks post injury)

A

Inflammatory cells will be replaced by fibroblasts, tenocytes and small blood vessels, all of which will contribute to granulation tissue formation and tendon healing

129
Q

What occurs during the maturation phase of tendon healing? (Over 3 months post injury)

A

The disorganised collagen fibrils will begin to be reorganised and aligned and the number of fibroblasts will decrease

130
Q

What are tendon stretch lesions?

A

Tendon stretch lesions occur when the collagen fibrils are pulled out of their crimp arrangement leading to collagen fibril and capillary rupture

131
Q

What is one of the most common tendon injuries seen in racing thoroughbreds?

A

Superficial digital flexor tendon injury

132
Q

How does high intensity exercise accelerate the levels of microdamage preceding a superficial digital flexor tendon injury?

A

High intensity exercise causes mechanical overload, hyperthermia and hypoxia of the tendon which contribute to microdamage

133
Q

Why does high intensity exercise easily cause hyperthermia of the superficial digital flexor tendon?

A

Tendons convert both kinetic and potential energy into elastic energy, with 5-10% of this elastic energy being lost as heat. This can progress to hyperthermia with high intensity exercise as tendons have a poor vascular supply and thus a poor dissipation of heat.

134
Q

What are the early histological signs of tendon microdamage caused by exercise?

A

Decreased collagen crimp angle
Decreased collagen fibril diameter

135
Q

What are the early histological signs of tendon microdamage caused by ageing?

A

Decreased collagen crimp angle
Decreased cellularity

136
Q

What is the main sign of advanced microdamage of the superficial digital flexor tendon upon gross examination?

A

Red lesion within the core of the superficial digital flexor tendon

MODULE 7 - Skin and Bones (22 decks)

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