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MOD (year 3) > Orthopaedics > Flashcards

Orthopaedics Flashcards

1
Q

what cells are found in bone?

A

osteoclasts
osteocytes
osteoclasts

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2
Q

what is the bone matrix made of?

A

collagen

hydroxyapatite crystals

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3
Q

what is the function of bone?

A 
skeletal support
protection
haematopoesis
regulation of mineral homeostasis
fat storage
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4
Q

what is the precursor to bone in utero?

A

cartilage

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5
Q

what are the two types of bone?

A 
cortical 
cancellous bone (trabecular bone)
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6
Q

where is cancellous bone found?

A

metaphysis
flat bone
cuboidal bone

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7
Q

what is the function of cancellous bone?

A

dissipation of load

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8
Q

what process increased bone length?

A

endochondral ossification

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9
Q

what process is responsible for cuboidal bone development?

A

endochondral ossification

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10
Q

what is appositional growth?

A

increases length

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11
Q

what is longitudinal growth?

A

increase longitudinally

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12
Q

what is modelling?

A

alteration in the shape of the bone

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13
Q

what happens to the trabecular bone when load/exercise is increased?

A

increased thickness
increased bridging between trabeculae
(modelling by microfractures)

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14
Q

what is bone remodelling?

A

replacement of damaged bone

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15
Q

define anisotropic

A

describes how a substance responds to load depending on the speed it is loaded

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16
Q

what determines the mechanical properties of bone?

A

size/shape
magnitude of load
direction of load
rate of loading

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17
Q

what are the two responses to load?

A

elastic deformation

plastic deformation

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18
Q

what is elastic deformation?

A

with loading/unloading the bone deforms and returns to its original shape

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19
Q

what is plastic deformation?

A

with loading/unloading the bone deforms but doesn’t return to its original shape (microcracks, incomplete fractures…)

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20
Q

what does plastic deformation trigger?

A

bone remodelling

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21
Q

what is the consequences of repeated plastic deformation?

A

weakening of normal bone

complete failure of bone

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22
Q

what are three metabolic bone diseases?

A

parathyroid hormone abnormality
vitamin D deficiency
paraneoplastic

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23
Q

what is developmental orthopaedic disease?

A

group of diseases of multifactorial aetiology resulting in musculoskeletal problems

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24
Q

where does endochondral ossification occur?

A

metaphysical growth plate

articular-epiphyseal cartilage complex

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25
Q

what are the stages seen at the growth plate?

A 
resting cartilage
proliferative cartilage 
hypertrophic cartilage
calcifying cartilage
secondary spongiosa
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26
Q

what is required for cartilage to mineralise?

A

blood supply

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27
Q

what ways can endochondral ossification malfunction at the physical growth plate?

A

abnormal deposition of matrix
abnormal mineralisation
poor conversion of bone
retention of cartilage

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28
Q

what is the results of endochondral ossification malfunction at the physical growth plate?

A

slow growth

uneven growth

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29
Q

what ways can endochondral ossification malfunction at the articular-epiphyseal cartilage complex?

A

abnormal deposition of matrix
abnormal mineralisation
retention of cartilage

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30
Q

what is the results of endochondral ossification malfunction at the articular-epiphyseal cartilage complex?

A

slow growth
uneven growth
cartilage flaps

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31
Q

what is chondrodysplasia?

A

dwarfism

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32
Q

what is osteochondrosis?

A

general term to describe abnormalities of cartilage within a joint

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33
Q

what is osteochondritis?

A

inflammation of the cartilage within a joint

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34
Q

what is osteochondrosis/osterochondritis dissecans?

A

the formation of cartilaginous or osteochondral flaps and undulations

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35
Q

what is OCD?

A

osteochondritis dissecans

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36
Q

when can abnormalities occur to cause osteochondritis dissecans?

A

disruption of blood supply
abnormal chondrocyte maturation
defective matrix production
persistence of hypertrophic chondrocytes

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37
Q

what does OCD lead to?

A

thickened retained hypertrophic cartilage

disruption to the subchondral bone plate

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38
Q

how can disrupted blood supply lead to OCD?

A

affects the mineralisation of the bone altering the biochemical and biomechanical properties of bone

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39
Q

what is the first clinical sign of OCD?

A

effusions (swelling of the joint)

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40
Q

what are some risk factors for OCD?

A

rapid growth (cattle/pigs)
genetics
nutrition
trauma

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41
Q

what nutritional influence effect OCD?

A

excess energy/protein

imbalances in calcium and phosphate

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42
Q

what can untreated OCD result in?

A

osteoarthritis

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43
Q

how does OCD appear on radiographs?

A 
irregular subchondral bone
osseous densities (fragments in joint)
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44
Q

what are some developmental orthopaedic diseases of horses?

A

osteochondrosis
physitis
angular limb deformities
flexural deformities

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45
Q

what are some developmental orthopaedic diseases of dogs?

A

osteochondrosis
hypertrophic osteodystrophy
legg calve perthes
hip dysplasia

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46
Q

what are some developmental orthopaedic diseases of cows?

A

osteochondrosis

flexural deformities

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47
Q

what are some developmental orthopaedic diseases of pigs?

A

osteochondrosis

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48
Q

what can cause subchondral cyst like lesions?

A

abnormal endochondral ossification (collapse)

trauma of articular cartilage and SC bone

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49
Q

what is physitis?

A

enlargement of the physis through inflammation and disrupted endochondral ossification

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50
Q

what are the clinical signs of physics?

A

lameness

stiff gait

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51
Q

what aged dogs does hypertrophic osteodystrophy occur in?

A

2-8 month old (large breeds)

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52
Q

what is the pathogenesis of hypertrophic osteodystrophy?

A

necrosis of the capillary loops of the cartilage of the metaphysical physis leads to a cuff of metaplastic cartilage

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53
Q

what are the clinical signs of hypertrophic osteodystrophy?

A

lameness, pain
fever
(bilateral and symmetrical)

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54
Q

what radiographic abnormalities are seen in dogs with hypertrophic osteodystrophy?

A

abnormal bone on diaphysial side of physis
decreased radio density parallel to physis
irregular widening of physis

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55
Q

what is done to treat hypertrophic osteodystrophy?

A

self limiting

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56
Q

what type of bones is effected by hypertrophic osteodystrophy?

A

long

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57
Q

what age dogs are effected by panosteitis?

A

5-18 months old (large breeds)

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58
Q

what type of dogs are most effected by panosteitis?

A

rapidly growing large breeds (males)

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59
Q

what is the pathogenesis of panosteitis?

A

increased osteoblastic and fibroblastic activity leads to fibrosis of bone tissue

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60
Q

what are the clinical signs of panosteitis?

A

acute shifting lameness and pain

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61
Q

what radiographic abnormalities are seen of dogs with panosteitis?

A

increased opacity of medullary cavity
indistinct trabecular pattern
increased endosteal opacity

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62
Q

what is done to treat panosteitis?

A

self limiting

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63
Q

what aged dog is legg calve perthes disease seen in?

A

4-11 months (toy breeds)

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64
Q

what is the pathogenesis of legg calve perthes disease?

A

avascular necrosis of the femoral head leads to collapse of the of the articular surface

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65
Q

what are the clinical signs of legg calve perthes disease?

A

acute onset lameness

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66
Q

what are the radiographic abnormalities seen with legg calve perthes disease?

A

osteolysis of femoral head
collapse and thickened femoral neck
fractures

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67
Q

what are the two dysplasia seen in dogs?

A

hip and elbow

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68
Q

what causes hip dysplasia in dogs?

A

abnormal anatomy of femoral head and acetabulum

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69
Q

what are the two types of angular limb deformities?

A

valgus (lateral)

varus (medial)

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70
Q

what are the potential locations of angular limb deformities in horses?

A

metaphysical growth plate
epiphysis
cuboidal bones
metaphysis

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71
Q

what dog breeds are predisposed to angular limb deformities?

A

small breeds (ShihTzu)

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72
Q

what causes angular limb deformities in dogs?

A

differential growth between bones - radius and ulna - (generally due to damage/trauma to toroth plates)

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73
Q

what causes flexural deformities of horses and cows?

A

disproportionate growth of tendons and its associated skeletal muscles

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74
Q

in horses, what fractures result in immediate euthanasia?

A

complete femur fracture
complete humorous fracture
complete tibia fracture
open, unstable fractures

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75
Q

how should horses with forelimb injuries be transported?

A

facing backwards

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76
Q

how should horses with hindlimb injuries be transported?

A

facing forwards

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77
Q

what rule must be followed when splitting a fracture?

A

stabilise joint above and below

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78
Q

what are compound fractures?

A

open (breaks the skin)

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79
Q

what are the three types of compound fracture?

A

1 - bone punctures through skin (treat as closed)
2 - open but minimal soft tissue damage and bone loss
3 - significant tissue damage and bone loss

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80
Q

what is a fracture?

A

disruption in the cortical continuity of bone (complete/incomplete)

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81
Q

what are the 4 As?

A

alignment
apposition
apparatus
activity

82
Q

what does alignment mean regarding fracture repair?

A

joints need to be in line

83
Q

what must be done when correcting a fracture surgically?

A

appose the forces acting on the fracture

84
Q

what fractures are transverse?

A

any up to 30 degrees

85
Q

what needs to be included when describing a fracture?

A 
open/closed
bone
position
fracture line
degree of displacement
86
Q

what ways can the position of a fracture be described?

A

articular
epiphyseal
growth plate
diaphyseal

87
Q

how can fracture lines be described?

A 
transverse
oblique
spiral
comminuted
segmental
88
Q

what are avulsion fractures?

A

small pieces of bone pulled off at the point of tendon attachment

89
Q

what classification system is used for growth plate (physeal) fractures?

A

salter-harris (I-VI) - lower the number the better the prognosis

90
Q

what is a type I salter-harris fracture?

A

straight across the physis

91
Q

what is a type II salter-harris fracture?

A

across physis and out through metaphysis

92
Q

what is a type III salter-harris fracture?

A

across physis and out through articular surface

93
Q

what is a type IV salter-harris fracture?

A

from articular surface through the growth plate to metaphysis

94
Q

what are the two types of bone healing?

A

primary (direct)

secondary (indirect)

95
Q

what are the stages of secondary fracture healing?

A 
haematoma
granulation tissue
connective tissue
fibrocartilage
bone formation (callus)
callus remodelling
96
Q

what has to be done for direct bone healing to take place?

A

bone compressed against each other

97
Q

what factors influence the healing on fractures in a positive way?

A 
young patient (<8 months)
healthy
closed fracture
low energy
single injury
closed reduction
non-articular
98
Q

what are the only fractures suitable for casting?

A

transverse fracture on the distal limb

99
Q

what is the only force IM pins oppose?

A

bending

100
Q

what are the disadvantages of IM pins?

A

poor at resting rotation or shear (shouldn’t be used on their own)
interfere with medullary blood supply

101
Q

what is the aim of cerclage wire?

A

give tight compression to bone

102
Q

what fractures should cerclage wire be used for?

A

long oblique fractures

103
Q

what are the uses of positional screws?

A

maintain relative position of two bone fragments
fasten plate to bone
anchor wire/suture to bone
lock an interlocking nail

104
Q

what are lag screws used for?

A

create compression between bones (larger hole in near cortex so its pulled together)

105
Q

what are the indications for external fixators (ESFs)?

A 
long bone fractures
highly comminuted fractures
adjacent to other fractures
open/infected fractures
immobilising joints for soft tissue repair
corrective osteotomies
106
Q

what are the advantages of external fixators?

A

inexpensive

can adjust fracture after surgery

107
Q

what is required for articular fracture healing?

A

rigid fixation

early return to function (range of motion, avoid atrophy)

108
Q

why is lameness in cattle important?

A 
welfare (pain)
public perception
milk loss
reproductive loss 
increased culling
nutrition (reduce DMI)
costs
109
Q

what is the first step of managing lameness in cattle?

A

being able to measure it (mobility scoring and lesion recording)

110
Q

what can hock scoring be used for?

A

determining how comfortable the environment is - predisposes to lameness

111
Q

what is the proximal phalanx also known as?

A

fetlock bone

112
Q

what is the middle phalanx also known as?

A

pastern bone

113
Q

what is the distal phalanx also known as?

A

pedal bone

114
Q

what is the lamellae of the cows foot?

A

leaflets of horn lining the inside of the wall

115
Q

what is the laminae of the cows foot?

A

leaflets of connective tissue, collagen fibres, blood vessels and nerves that fit between the lamellae

116
Q

what is the suspensory apparatus of the cows foot?

A

collagen fibres keeping the pedal bone and dermal lamellae attached

117
Q

which claw of the hindlimb of cattle outgrows the other?

A

lateral outgrows the medial

118
Q

what are the two methods of foot trimming in cows?

A

5 step dutch method

dairyland method

119
Q

how long should the dorsal wall length be trimmed to in cattle feet?

A

8cm (depending on size)

120
Q

what should the sole depth at the toe be when trimming cattle feet by the dutch method?

A

7mm

121
Q

what are arthritides?

A

conditions causing pain/dysfunction to joints

122
Q

what is arthritis?

A

inflammation/degeneration of a joint

123
Q

what is a diarthrodial joint?

A

specialised joint consisting of a synovial cavity allowing articulation of two or more bones

124
Q

what is osteoarthritis?

A

degenerative condition ultimately leading to cartilage breakdown and loss of function

125
Q

what is the function of a diarthrodial joint?

A

allow frictionless pain free motion

126
Q

what makes synovial fluid?

A

ultrafiltration of plasma plus protein (hyaluronic acid)

127
Q

what covers articular bones at joints?

A

hyaline cartilage

128
Q

what makes up the fibrous joint capsule?

A

synovial membrane
nerves/blood vessels
supportive ligaments/tendons

129
Q

what is articular cartilage made of?

A

extracellular matrix with some articular chondrocytes

130
Q

what is responsible for the maintenance of the matrix of articular cartilage?

A

chondrocytes

131
Q

what is osteoarthritis a disease of?

A

articular cartilage (other tissue also contributes)

132
Q

what are some predisposing factors for osteoarthritis?

A 
exercise/trauma
developmental orthopaedic disease
obesity
genetics
sepsis
repeated medication
ageing
133
Q

what are the radiographic signs of osteoarthritis?

A 
soft tissue swelling
osteophytosis 
enthesiophytosis 
subchondral bone sclerosis 
intra-articular mineralisation
fragmentation
joint space collapse
subchondral bone cyst
134
Q

what is osteophytosis?

A

new bone formation around the joint margin

135
Q

what is enthesiophytosis?

A

new bone formation within soft tissue around the joint

136
Q

what are the aims of osteoarthritis therapy?

A

analgesia
control articular inflammation
limit damage to articular tissue
promote healing

137
Q

what is conservative therapy of osteoarthritis?

A

rest/restrict activity
weight loss
exercise (care)

138
Q

what can be used to treat osteoarthritis medically?

A

NSAIDs
corticosteroids
hyaluronic acid
bisphosphonates

139
Q

what are the three effects of NSAIDs?

A

anti-inflammatory
anti-pyretic
analgesic

140
Q

how do NSAIDs work?

A

by COX inhibition

141
Q

how do corticosteroids work?

A

bind to cytoplasmic and nuclear receptors - inhibit cytokines and alter signalling pathways

142
Q

what effects does hyaluronic acid have on joints?

A

replaces synovial fluid
anti-inflammatory
analgesia

143
Q

what effect do bisphosphonates have on joints?

A

inhibits bone resorption by inhibiting osteoclasts

144
Q

what surgical treatments can be used for osteoarthritis?

A

arthroscopy (decried/flush)
joint replacement
arthrodesis

145
Q

how does immune-mediated joint disease present?

A

polyarthritis (erosive/non-erosive)

146
Q

what are most immune mediated joint diseases due to?

A

abnormal/inapproriate activity of immune cells and antigen presentation

147
Q

what is the main part of the joint effected by immune mediated joint diseases?

A

synovium

148
Q

what are the clinical signs of immune mediated joint diseases?

A

multiple limb joint pain/swelling, stiffness, lameness, pyrexia of unknown origin

149
Q

what is the predominant cell seen following synoviocentesis of immune mediated joint diseases?

A

high neutrophil count

150
Q

what changes to the blood could suggest an immune mediated joint disease?

A 
anaemia
leucopenia
thrombocytopenia 
raised globulins
low albumin
151
Q

what drugs can be used to treat immune mediated joint diseases?

A

corticosteroids

152
Q

what are some causes of infective arthritis?

A

bacteria - haematogenous, trauma/wound, iatrogenic

153
Q

what is the response to infective arthritis?

A

marked inflammation - vasodilation and neutrophil influx with inflammatory cytokine/enzyme release

154
Q

how does normal synovial fluid appear?

A

pale yellow and viscous

155
Q

how does septic synovial fluid appear?

A

serosanguineous, turbid and reduced viscosity, increased volume

156
Q

what is done to treat septic arthritis?

A

treat un darling cause
systemic/local antimicrobials
remove inflammatory mediators (lavage)

157
Q

what causes Lyme disease?

A

Borrelia burgdorferi

158
Q

how do dogs with Lyme disease present?

A

inflammatory non-erosive arthropathy
shifting lameness
swollen joints

159
Q

what is used to treat Lyme disease?

A

doxycycline

160
Q

what are the functions of tendons?

A

transfer force from muscle to bone (movement)
supports joint
store energy

161
Q

what are the functions of ligaments?

A

attach/stabilise joints
protect tendons
proprioception

162
Q

what is responsible for the maintenance and degradation of tendon/ligament extracellular matrix?

A

tenocytes/ligamentocytes

163
Q

what are the two types of injury to tendons/ligament?

A

extrinsic (trauma)

intrinsic (overload/degeneration)

164
Q

what should be assessed when ultra sounding tendons/ligaments?

A 
change in cross-sectional area
fibre echogenicity
margination
position
focal lesions vs generalised
acute vs chronic 
blood flow (doppler)
165
Q

define anechoic

A

no echogenicity (black)

166
Q

define hypoechoic

A

reduced echogenecity

167
Q

what are the three phases of tendon/ligament injury repair?

A

inflammatory
proliferative
remodelling

168
Q

what are the clinical signs of the acute inflammatory phase of tendon/ligament injury?

A

lameness
pain
heat
swelling

169
Q

what pathological changes are seen during the acute inflammatory of tendon/ligament injury?

A

haemorrhage

inflammation (neutrophils, macrophage, oedema, increased blood flow)

170
Q

what treatment can be used for the acute inflammatory phase of tendon/ligament injury?

A 
cold therapy/NSAIDs (limit inflammation)
supporting bandage (limit further damage)
171
Q

what clinical signs are associated with proliferative phase of tendon/ligament injury?

A

reduced lameness
resolution inflammation
tendon enlarged

172
Q

what pathological changes are seen during the proliferative phase of tendon/ligament injury?

A

angiogenesis

fibroplasia (fibroblasts and collage)

173
Q

what treatment can be given during the proliferative phase of tendon/ligament injury?

A

splinting and stem cells (promote angiogenesis)
stem cells and physiotherapy (minimise scar formation)
exercise

174
Q

what can be done if a tendon/ligament has been lacerated?

A

repair ends if feasible

175
Q

what can be done if a tendon/ligament is part of an avulsion fracture?

A

reattach and cast

176
Q

what are the clinical signs of chronic muscle injury?

A

stiffness, cramping, pain, atrophy, fibrosis/calcification

177
Q

what biochemistry can be used in the diagnosis of muscle conditions?

A

serum muscle enzymes (CK/AST)

urine (myoglobin)

178
Q

what is CK in relation to serum muscle enzymes?

A

creatinine kinase

179
Q

what diagnostic tools can be used for muscle conditions?

A

biochemistry
ultrasound
muscle biopsy

180
Q

what is atrophy?

A

reduction in size

181
Q

what can cause muscle atrophy?

A

disuse
denervation
cachexia

182
Q

what are some causes muscle denervation?

A 
trauma (laryngeal hemiplasia)
Myasthenia gravis (neuromuscular junction defect)
183
Q

what must stay intact for a nerve to be able to reinnervate?

A

nerve sheath

184
Q

what is muscular hypertrophy?

A

increased muscle bulk due to larger fibres (increased workload)

185
Q

what are the three main types of muscular degeneration?

A

cellular swelling
hyaline degeneration
granular degeneration

186
Q

what can cause cellular swelling of muscles?

A

minor chemical imbalances within the muscle (Na/K)

187
Q

what does hyaline degeneration of muscles effect?

A

sarcoplasm

188
Q

what myopathy often causes hyaline degeneration?

A

nutritional myopathy

189
Q

what happens if there is irreversible damage to muscle tissue?

A

calcification

190
Q

how is circulatory disturbances to muscle compensated?

A

collateral circulation

191
Q

what causes white muscle disease?

A

selenium/vitamin E deficiency

192
Q

what are the clinical signs of white muscle disease?

A

muscle weakness/stiffness
recumbency
arrhythmia/murmur if myocardial effected

193
Q

what species is white muscle disease seen in?

A

cattle (calves)

194
Q

what causes stiff lamb disease?

A

selenium/vitamin E deficiency

195
Q

what is exertional rhabdomyolysis due to?

A

unfit horses (not been excised over the weekend)

196
Q

what are the clinical signs of acute exertional rhabdomyolysis?

A

stiffness to severe pain

197
Q

what muscles is acute exertional rhabdomyolysis seen in most commonly?

A

gluteal
semitendinosus
semimembranosus

198
Q

what dog breeds is eosinophilic myositis seen in?

A

large breeds (German shepherds)

199
Q

what muscles are effected by eosinophilic myositis?

A

temporal/masticatory muscles (enlarged)

200
Q

what is used to treat eosinophilic myositis?

A

corticosteroids

201
Q

what animals is atypical myoglobinuria seen in?

A

horses

202
Q

what are the clinical signs of atypical myoglobinuria?

A

fatal
muscle weakness/recumbency
increased CK/AST
(widespread necrosis)

MOD (year 3) (45 decks)

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