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VSCI300 MOD > Bones > Flashcards

Bones Flashcards

1
Q

what is the ft of bones

A 
structure
movement
satbility
protection
fat store
haematopoeisis
mineral homeostasis
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2
Q

lamella bone =

A

mature. organised long fibril sheets.

osteons, haversian systems, canaliculi

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3
Q

woven bone =

A

immature. dissorganised short fibril sheets

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4
Q

what sectiion of the bone has the most compressive forces? and what part is designed to dissipate most

A 
cortex
metaphyseal trabecular (woven bits) arranged to dissipate force
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5
Q

what is micro-modelling

A

modelling of trabeculae to suit disspation of forces upon it

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6
Q

how many cycles of exercise is required to stimulate remodelling?

A

36 cycles, recovers after 8hrs

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7
Q

if there is v rapid stimulation of current bone what happens

A

fibrolamellar bone laid down around the vessels - weak. after time, this bone is replaced by lamellar bone which includes osteons around the b vessels instead

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8
Q

briefly describe the process of remodelling

A

damage bone removed by oc

1ry osteons form in cortex and trabeculae thicken and align in medulla

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9
Q

how long does it take for OC to remove none?

A

4wks

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10
Q

how long does it take OB to replace bone?

A

3 mths

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11
Q

describe the 6 types of fracture

A
  1. transverse - bending
  2. oblique - compressive
  3. spiral - torsion
  4. comminuted - high impact
  5. open - pierce skin
  6. closed - wi surrounding ST
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12
Q

descr stress remodelling

A

RSI (36x ++)
remodelling - fibrolamella laid down but then trabeculae resorbed to be remodelled into correct alignment
–> inc porosity and decr stiffness and strength
= failure likely

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13
Q

descr modified equine trainig

A

use gallop short bursts more

train to inc bone mass on dorsal and both lateral aspects (cf more medial increases)

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14
Q

why are greyhounds left at and right medial carpal/tarsal bones thickeded?

A

always run counter clockwise - matches the loading

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15
Q

what injury does poor equine training predispose them to?

A

thick dorsal and palmar MCB/MTB due to rapid appositional growth–> f#
3rd C/T bone f# along trabceulae

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16
Q

how can growth be stimulates

A

GH
genes
load

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17
Q

what is necessary in the development of bone to allow mineralisation

A

blood supply!

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18
Q

at what 2 area will endochondral ossification start from

A

GP in either physis of epihysis

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19
Q

why does the thickness of the trabecular increase liklihood of fracturing

A

because it cant absorb as much

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20
Q

what is fibrolamellar bone

A

weak, poorly mineralised

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21
Q

if deformation is elastic what changes happen? and if its plastic deformation - what changes happen then

A

elastic - rtns to normal when f removed. stimulates Modelling to increase stiffness and strength
plastic - permenantly changed after and REmodelling stimulated (pos due to microcracks etc)

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22
Q

why would a physiological load on bone cause a fracture

A

becuase it was diseased

  • non-adaptive remodelling on eq/canine athlete
  • metabolic bone dz (hyperPTH or vitD defic)
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23
Q

what are the causes of MBD

A

hyperPTH (removes Ca+ form bone)
vit d deficiency - not abs from GIT well, not reabs from kidney and not converted
diet or dz

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24
Q

name an eq disease of flat bone reabsorption (clue - california)

A 
pulmonary silicosis = bone fragility syndrome
flat bones (scapular mainly), also leads to respir. dz
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25
Q

what is feline osteodystrophy

A

destruction of nasal turbinates

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26
Q

what hormone might help osteoporosis

A

oestrogen

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27
Q

what are the 3 main aetiopatholigies are

A

abn endochondral ossification
abn maturation of cartilage
inappropriate relative growth

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28
Q

name some common ortho dz in the horse

A

osteo-chondrosis
physitis
angular limb deformities
flexural deform

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29
Q

name som ecommon canine ortho dz

A

osteochondrosis (re anconeal process, fragmented medial coronoid process)
hypertrophy psteodystrophy
legg-calves perthes
hip dysplasia

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30
Q

what do pigs get ortho dz-wise

A

osteochondrosis

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31
Q

what ortho dz do bovids get

A

osteochondrosis and flexural deformities

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32
Q

endochondral ossification happens at the metaphyseal GP and epiphyseal in initial development, however _______ should be fully ossified at birth

A

metaphyseal

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33
Q

when are cuboidal bones developed

A

by 3wo

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34
Q

at the GP (physis) what histological layers are there.

A
  1. restin cart
  2. prolif cart
  3. hypertrophic (swells)
  4. calcifcation zone (burst and mineralises)
  5. 2ry spongiosa - which gets reabs and modelled etc.

*** the resting cartilage is ‘above’ the new bone ( as its getting pushed upwards and bone grows underneath the cartilage)

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35
Q

what EC abn are there

A
  • affect rate of growth
  • directionof growth
  • health are articular cart
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36
Q

what is osteochondrosis

A

chondrodysplasia (abn EC ossif)

results in thick retained hypertrophic cartilage

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37
Q

what is the pathogenesis of OCD (osteochondrosis)

A
  • disruption of blood supply
  • abn chondrocytes maturation
  • defective matrix production
  • persistence of hypertrophic chondrocytes (havent bURST AND CALICIFED)
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38
Q

if blood supply is disrupted, what is the result

A

impaired ability to withstand shearing forces

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39
Q

what is the patho-physiology of OCD

A

shearing forces cause separation of bone at osteochondral jct
cartilage flaps and fragmentation
exposed subchondral bone (eburnation)

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40
Q

clinical signs of OCD

A

arthritis

lameness

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41
Q

what is the aetiology of OCD

A

rapid growth - diet (incP:Ca balance; dec Cu:Zn balance), breed
+ trauma
hormones - test, GH, hyperinsulinaemia and hypothyroidism

42
Q

what are subchondral cyst-like lesions

A

abn EC ossification from leaving the cartilage core - when it collapses = ‘cyst-like’ lesion

43
Q

what is physitis and is it a concern

A

inflm or disruption of EC oss leading to lameness and stiffness

no -SELF LIMITING

44
Q

What is hypertrophic osteodystrophy and what causes it? (dogs)

A

2-8mo, large breeds
cause - CDV infection, bacterial infection, XS vit+min,
pathogenesis - necrosis of metaphyseal vasculature

45
Q

what are the signs of hypertrophic osteodystrophy

A

lame, fever, lethargy, pain
bilat and symmetrical lesions of long bones
abn diaphyseal bone, widened physis
SELF LIMITING

46
Q

what is panosteitis and when does it occur and why

A

idiopathic cause
5-18mo
rapid growing large breeds
fibrosis of bone tissue (BM, endosteum and periosteum)

47
Q

what are the signs of panosteitis (clinical and xray)

A

lame, shifting, lethargy, pain
inc medullary opacity, poor definition of trabeculae
SELF LIMITING

48
Q

what is legg-calve perthes

A

4-11 mo toy breeds
idiopathic
avascular necrosis of the fem head, if the sub-chondral bone loses stability it collapses

49
Q

what are the signs of legg-calve perthes

A

acute lameness, fracture of femoral head

osteolysis of fem head

50
Q

what is the reason of hip dysplasia

A

genetic laxity of joint lig (lig of the head of the femur)

51
Q

what causes the canine elbow dysplasia complex

A
  • un-united anconeal
  • OCD of humorous
  • fragm coronoid process
52
Q

what is shetland shoulder syndrome

A

abn humoural head + glenoid capsule

53
Q

in angular limb deformities there is a word for both medial and lateral defomity - what are they

A

medial - varus

lateral - valgus

54
Q

where might angular limb deformities happen

A 
metaphyseal GP
epiphyseal GP
cuboidal bones
metaphysis 
soft tissue laxity
55
Q

what canine breeds get angular limb deformities

A

small - shitzhu

56
Q

what is the reason behind canine angular limb deformities

A

asynchronous growth

57
Q

what are the reasons behind flexoid limb deformities

A

disproportionate growth bw muscle/tendon and bone

58
Q

what are the 2 forms of flexural limb deformity

A

congenital - neonate foals

acquired - rabidly growing foals, acute or chronic

59
Q

what maj condition does osteochondrosis lead to

A

osteoarthritis

60
Q

what is ‘arthritides’

A

conditons causing pain and dysfct of joints

61
Q

what is seen with OA

A

dec pH, hypoxia, and dec IL-1 (and other inflm mediators prod by synovium)
–> causes MMP to be released and enzymes to break down cartilage
xray - osteophytes, enthesiophytes, SCB sclerosis

62
Q

what are o-phytes

A

bone on joint margins

63
Q

what are enthesiophytes

A

bone on ST insertion

64
Q

what is sclerosis of the sub-endochondral bone

A

loses trabecular bone pattern

65
Q

how do you tx OA

A

analgesia, reduce inflm (NSAIDs to reduce PGE2 and No released from synoviocytes or csteroids), limit articular damage (cartofen vet helps proteoglycan synth) and help healing if pos (HA+csteroids)

66
Q

why shouldnt NSAIDs be used in wound healing

A

inhibit PMN migration

67
Q

what surgical options are there for OA

A

arthrodesis - destroy cartilage and fuse

arthroscopy - assess, debride and replace joint

68
Q

name some tx that are less well known, but used for joint diseases

A

bisphosphonates - antag against IL
poly-unsta FA - to reduce arachidonic acid (cod liver oil)
glucosamine/chondroitin - reduce PGE and NO
avocado, soya bean, vit+min - reduce IL and PGE2

69
Q

desc the disease of IM-polyarthritis

A

chronic Ag stim and IC formed at the synovio-cytes
pyrexia, lethargy and joint swelling, shifting lameness
can be erosive (poor px)
and ead to 2ry OA

70
Q

how is IM polyarthritis treated

A

csteroids (cyclosporin and azathioprine)

71
Q

desc the process of disease of infective arthritis

A

bacteria in to joint
cause inflm, inc fluid, joint effusion, capillary dilation and release reactive O2spp which all damages the synovium more.
bacteria hide in synovium + fibrin clots = chronic inflm
–> OA

72
Q

how do you dx septic arthritis

A

synovio-centesis = get EDTA (TP and WBCC) and plain (C+S)

73
Q

when might an septic arthritis not cause lameness

A

if its draining

74
Q

what does lymes dz cause (borellia)

A 
shifting lameness (D) = non-erosive arthrpathy. 90% PMN in the synoviocentesis
tx - doxycycline
75
Q

what are tendons made of

A

type1 collagen

76
Q

what are ligaments made of

A

90% type1; 10% type2 collagen

77
Q

which is more serious - flexor or extensor tendon injuries? why?

A

flexor

high loads and E stored, if lacerated - cant heal well wi the sheath. (50% heal rate)

78
Q

what is the most common soft tissue injury of the horse

A

SDFT (90%)

79
Q

what does the SDFT do

A

support fetlock and store E

80
Q

how hot does a tendon get at gallop

A

45 degrees, and 17% strain (yet it can fail at only 10%)

81
Q

what is the manica flexoria

A

part of the SDFT that wrap around the DDFT as it goes through the fetlock canal (when the SDFT is outside, not inside)

82
Q

what would you see in u/sound

A

reduce echogenicity

83
Q

learn the SDFT and DDFT look like on ultra-sound and all the -itis-es

A

sorry….

84
Q

what is seen on u/sound in SDFT tendonitits

A

focal an-echoic lesions
loss of borders
swelling
(fetlock sinking and lameness)

85
Q

how do you tx tendonitis

A 
cold hose
box rest
NSAIDs
support dressings
neurectomy
86
Q

what is the accessory lig to the DDFT

A

check ligament

87
Q

how do you tx a desmitis

A

cold hosing, box rest - also pos desmotomy
stem-cells and PLT-rich plasma
shockwava therapy
neurectomy

88
Q

why is the px annular sheath (at level of sesamoids) sometimes cut ‘desmotomy’

A

because if the flexor tendons in the sheath are inflm - cant expand = more pain than nec

89
Q

where is it that the patella gets ‘hooked’ when locked

A

med trochlear ridge - quads unlock it

90
Q

what causes gastrocnemius rupture

A

rotation force (foot stuck) por px

91
Q

what are the signs of peroneus tertias rupture

A

stifle flex AND hock ext (not okay..) poor px

92
Q

how does the SDFT luxate

A

inserts on the tuber calci on calcanean process so luxate = falling off - lateral trauma

93
Q

name some equine myopathies

A
  • neurogenic atrophy (motor neurone dz)
  • white muscle dz (vitE;Se)
  • acute or chronic exertional rhabdomyolysis (unfit, calm down)
  • non-exertional rhabdomyolysis (clostridia or inj-site abscess)
  • atypical myoglobinuria (sycamore)
94
Q

what are the fracture classifications for open fractures

A

grade 1 = bone was out, but now back in
grade 2 = bone outside, neither bone nor ST missing
grade 3 = missing bone and ST

95
Q

2 common avulsion fractures are…

A 
lat malleolus (ulna)
tibial tuberosity (tibia)
96
Q

desc the basic fracture healing process

A
  • form clot (200% strain)
  • dev inflm and oedema
  • cell proliferation
  • cartilage and bone for = callus dev
  • —for callus to form the strain must be
97
Q

where does the blood suppy for fx healing come from - as it will have lost most of the medullary arterial supply

A

surrounding ST AND the periosteal arteries (dont lose any periosteum)

98
Q

fracture can heal either directly or indirectly - desc brief differences

A

direct -

99
Q

how can you achieve external co-aptation

A 
IM pins
cerclage wires
screws - lage and positional
plate - compression, neutral, buttress
external fixators - good if highly communited
100
Q

what is the ideal lavage

A

19G, 100ml/g in a 20ml syringe

101
Q

what banages are good for intial assessment

A

wet-dry and silver and hydrogel

VSCI300 MOD (32 decks)

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